Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0085437 (
bacterial meningitis
)
4,038
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Although people with
bacterial meningitis
lack adequate protective antibody against the invading pathogen, most do not have an underlying immunodeficiency. Certain comorbid conditions increase the risk for development of bacterial sepsis and meningitis. In addition, certain congenital complement deficiencies, defects of antibody production, or asplenia may be first recognized by the occurrence of
bacterial meningitis
, particularly when it occurs in infants or young children. Deficiencies of the terminal components of complement (C5-C9) or
properdin
have been associated with recurrent or invasive neisserial infections, and asplenia, agammaglobulinemia, and deficiencies of the early components of complement (e.g., C1-C3) are associated with risks of infections caused by Streptococcus pneumoniae, Haemophilus influenzae, and meningococci. The presence of congenital or acquired immunodeficiencies should be considered in persons who present with
bacterial meningitis
on the basis of the etiology, clinical epidemiology, and presence of other risk factors.
...
PMID:Indications for the immunological evaluation of patients with meningitis. 1252 51
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.
...
PMID:[Complement protein hereditary deficits during purulent meningitis: study of 61 adult Tunisian patients]. 1938 94
Meningeal defects and primitive ENT infections are known to promote pneumococcal meningitis. Other risk factors can be identified in the occurrence of community acquired
bacterial meningitis
(CABM) and play a key role either in the frequency of this kind of infection, the type of bacteria concerned, the prognosis or the risk of recurrence. Thus, epidural infiltrations are rarely responsible for staphylococcal or streptococcal meningitis. Cochlear implants are also known to increase the risk of pneumococcal meningitis. The occurrence in children of aseptic meningitis or meningitis due to Staphylococcus aureus or Enterobacteriaceae is strongly suggestive of congenital spinal or cerebral anomalies (dermal sinus or spina bifida). MRI must be rapidly performed. In cases of splenectomy or asplenism, pneumococcal meningitis is common and must be prevented. According to the larger series available on this topic, age over 60, diabetes mellitus, alcoholism and immune deficiency are found to promote CABM in about 25% of cases. Streptococcus pneumoniae is the most frequent causative bacteria in elderly patients, in case of alcoholism, as well as Listeria monocytogenes and some Enterobacteriaceae (Escherichia coli, Klebsiella pneumoniae). L. monocytogenes is frequently isolated in immunodepressed patients and patients treated by anti-TNF molecules (infliximab notably). Finally, some genetic polyphormisms promote CABM: complement and
properdin
deficiencies (meningococcal meningitis), mannose-binding lectin deficiency, Fcgamma receptors alteration or interleukin-1 and IL-1R polymorphisms. Screening for such genetic disorders may be discussed in case of CABM but is mandatory in case of recurrent meningococcal infections.
...
PMID:[Predisposing factors of community acquired bacterial meningitis (excluding neonates)]. 1941 29