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Recurrent meningococcal disease

MedGen UID:
369692
Concept ID:
C1970263
Finding
Synonym: Increased susceptibility to Neisseria meningitidis infections
 
HPO: HP:0005381

Definition

Recurrent infections by Neisseria meningitidis (one of the most common causes of bacterial meningitis), which is also known as meningococcus. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVRecurrent meningococcal disease

Conditions with this feature

Complement component 5 deficiency
MedGen UID:
91003
Concept ID:
C0343047
Disease or Syndrome
A rare genetic disorder with an autosomal recessive pattern of inheritance. It is caused by the ineffective or decreased biosynthesis of the fifth complement component, C5. C5 deficiency may also be acquired acutely post-infection. If C5 is adequately synthesized, its rapid depletion may result in a functional deficiency. Clinical signs of the inherited deficiency present within the second decade of life and are consistent with the signs of recurrent systemic infection. Deficiency of serum C5 and its major cleavage product, C5b, a component of the membrane attack complex, increases susceptibility to Neisserial infections.
Complement component 7 deficiency
MedGen UID:
355270
Concept ID:
C1864694
Disease or Syndrome
Patients with C7 deficiency have an increased susceptibility to recurrent bacterial infections, especially meningitis caused by Neisseria meningitidis (Nishizaka et al., 1996).
Complement component 6 deficiency
MedGen UID:
436639
Concept ID:
C2676232
Disease or Syndrome
Any classic complement early component deficiency in which the cause of the disease is a mutation in the C6 gene.
Mannose-binding lectin deficiency
MedGen UID:
482216
Concept ID:
C3280586
Disease or Syndrome
Mannose-binding lectin (MBL) deficiency, defined as MBL protein level of less than 100 ng/ml, is present in about 5% of people of European descent and in about 10% of sub-Saharan Africans. Most MBL-deficient adults appear healthy, but low levels of MBL are associated with increased risk of infection in toddlers, in cancer patients undergoing chemotherapy, and in organ-transplant patients receiving immunosuppressive drugs, particularly recipients of liver transplants (review by Degn et al., 2011). MBL is a soluble molecule that can activate the lectin pathway of the complement system; deficiency may thus lead to defects in the complement system (summary by Garcia-Laorden et al., 2008). Genetic Heterogeneity of Lectin Complement Activation Pathway Defects See also LCAPD2 (613791), caused by variation in the MASP2 gene (605102) on chromosome 1p36, and LCAPD3 (613860), caused by variation in the FCN3 gene (604973) on chromosome 1p36.
Factor I deficiency
MedGen UID:
483045
Concept ID:
C3463916
Disease or Syndrome
C3 glomerulopathy (C3G) is a complex ultra-rare complement-mediated renal disease caused by uncontrolled activation of the complement alternative pathway (AP) in the fluid phase (as opposed to cell surface) that is rarely inherited in a simple mendelian fashion. C3G affects individuals of all ages, with a median age at diagnosis of 23 years. Individuals with C3G typically present with hematuria, proteinuria, hematuria and proteinuria, acute nephritic syndrome or nephrotic syndrome, and low levels of the complement component C3. Spontaneous remission of C3G is uncommon, and about half of affected individuals develop end-stage renal disease (ESRD) within ten years of diagnosis, occasionally developing the late comorbidity of impaired visual acuity.
Complement factor b deficiency
MedGen UID:
816280
Concept ID:
C3809950
Disease or Syndrome

Professional guidelines

PubMed

Gurevich E, Landau D
Paediatr Drugs 2023 Mar;25(2):193-202. Epub 2023 Jan 13 doi: 10.1007/s40272-022-00555-6. PMID: 36637720Free PMC Article
Carazo S, Skowronski DM, Brisson M, Barkati S, Sauvageau C, Brousseau N, Gilca R, Fafard J, Talbot D, Ouakki M, Gilca V, Carignan A, Deceuninck G, De Wals P, De Serres G
Lancet Infect Dis 2023 Jan;23(1):45-55. Epub 2022 Sep 21 doi: 10.1016/S1473-3099(22)00578-3. PMID: 36152671Free PMC Article
Dicks RA
Arch Dis Child Educ Pract Ed 2015 Oct;100(5):241. Epub 2015 Aug 11 doi: 10.1136/archdischild-2014-307964. PMID: 26264393

Recent clinical studies

Etiology

Andreoni J, Käyhty H, Densen P
J Infect Dis 1993 Jul;168(1):227-31. doi: 10.1093/infdis/168.1.227. PMID: 8515116
Figueroa J, Andreoni J, Densen P
Immunol Res 1993;12(3):295-311. doi: 10.1007/BF02918259. PMID: 8288947

Diagnosis

Owen EP, Würzner R, Leisegang F, Rizkallah P, Whitelaw A, Simpson J, Thomas AD, Harris CL, Giles JL, Hellerud BC, Mollnes TE, Morgan BP, Potter PC, Orren A
Mol Immunol 2015 Mar;64(1):170-6. Epub 2014 Dec 19 doi: 10.1016/j.molimm.2014.11.010. PMID: 25534848
Bols A, Janssens J, Peetermans W, Stevens E, Bobbaers H
Acta Clin Belg 1993;48(1):42-7. doi: 10.1080/17843286.1993.11718283. PMID: 8388602

Therapy

Andreoni J, Käyhty H, Densen P
J Infect Dis 1993 Jul;168(1):227-31. doi: 10.1093/infdis/168.1.227. PMID: 8515116

Prognosis

Bols A, Janssens J, Peetermans W, Stevens E, Bobbaers H
Acta Clin Belg 1993;48(1):42-7. doi: 10.1080/17843286.1993.11718283. PMID: 8388602

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