Details of Disease

Disease Name

Meningococcal meningitis

Definition

An acute bacterial disease caused by Neisseria meningitides that presents usually, but not always, with a rash (non blanching petechial or purpuric rash), progressively developing signs of meningitis (fever, vomiting, headache, photophobia, and neck stiffness) and later leading to confusion, delirium and drowsiness. Neck stiffness and photophobia are often absent in infants and young children who may manifest nonspecific signs such as irritability, inconsolable crying, poor feeding, and a bulging fontanel. Meningococcal meningitis may also present as part of early or late onset sepsis in neonates. The disease is potentially fatal. Surviving patients may develop neurological sequelae that include sensorineural hearing loss, seizures, spasticity, attention deficits and intellectual disability.

Disease Hierarchy

DISB38M8: Meningococcal infection

DISRP9SL: Bacterial meningitis

DISCKTAT: Meningococcal meningitis

Disease Identifiers

MONDO ID

MONDO_0018059

MESH ID

D008585

UMLS CUI

C0025294

MedGen ID

6299

Orphanet ID

33475

SNOMED CT ID

192644005

General Information of Disease (ID: DISCKTAT)

Drug-Interaction Atlas (DIA) of This Disease

Drug-Interaction Atlas (DIA)

This Disease is Treated as An Indication in 7 Approved Drug(s)

Drug Name	Drug ID	Highest Status	Drug Type	REF
Ampicillin	DMHWE7P	Approved	Small molecular drug	[1]
Cefotaxime	DMEB837	Approved	NA	[2]
Ceftazidime	DM41GRA	Approved	Small molecular drug	[3]
Ceftriaxone	DMCEW64	Approved	Small molecular drug	[4]
Chloramphenicol	DMFXEWT	Approved	Small molecular drug	[5]
Meropenem	DM62UHC	Approved	Small molecular drug	[6]
Sulfisoxazole	DMXLT8C	Approved	Small molecular drug	[7]
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⏷ Show the Full List of 7 Drug(s)

This Disease is Treated as An Indication in 1 Clinical Trial Drug(s)

Drug Name	Drug ID	Highest Status	Drug Type	REF
Benzylpenicillin	DMS9503	Phase 3	Small molecular drug	[8]
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Molecular Interaction Atlas (MIA) of This Disease

Molecular Interaction Atlas (MIA)

This Disease Is Related to 3 DTT Molecule(s)

Gene Name	DTT ID	Evidence Level	Mode of Inheritance	REF
TLR9	TTSHG0T	Limited	Genetic Variation	[9]
CFP	TTLA0VS	Strong	Biomarker	[10]
MMP13	TTHY57M	Strong	Biomarker	[11]
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This Disease Is Related to 1 DTP Molecule(s)

Gene Name	DTP ID	Evidence Level	Mode of Inheritance	REF
SLC11A1	DT650XW	Strong	Biomarker	[12]
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This Disease Is Related to 3 DOT Molecule(s)

Gene Name	DOT ID	Evidence Level	Mode of Inheritance	REF
C6	OTCKR304	Strong	Genetic Variation	[13]
C7	OTZ27VJN	Strong	Biomarker	[14]
C9	OT7I5FDX	Strong	Biomarker	[15]
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References

1	Ampicillin FDA Label
2	Cefotaxime FDA Label
3	Ceftazidime FDA Label
4	Ceftriaxone FDA Label
5	Chloramphenicol FDA Label
6	Meropenem FDA Label
7	Sulfisoxazole FDA Label
8	Meningococcal meningitis and diabetes insipidus. Scand J Infect Dis. 1988;20(3):341-3.
9	Analysis of TLR2, TLR4, and TLR9 single nucleotide polymorphisms in children with bacterial meningitis and their healthy family members.Int J Infect Dis. 2017 Jul;60:23-28. doi: 10.1016/j.ijid.2017.04.024. Epub 2017 May 6.
10	Molecular characterisation of 10 Dutch properdin type I deficient families: mutation analysis and X-inactivation studies.Eur J Hum Genet. 2000 Jul;8(7):513-8. doi: 10.1038/sj.ejhg.5200496.
11	Differential expression of matrix metalloproteinases in bacterial meningitis.Brain. 1999 Aug;122 ( Pt 8):1579-87. doi: 10.1093/brain/122.8.1579.
12	Iron and infection: effects of host iron status and the iron-regulatory genes haptoglobin and NRAMP1 (SLC11A1) on host-pathogen interactions in tuberculosis and HIV.Clin Sci (Lond). 2006 May;110(5):503-24. doi: 10.1042/CS20050273.
13	Complement component C6 deficiency in a Spanish family: implications for clinical and molecular diagnosis.Gene. 2013 May 25;521(1):204-6. doi: 10.1016/j.gene.2013.03.027. Epub 2013 Mar 26.
14	Familial deficiency of the seventh component of complement associated with recurrent bacteremic infections due to Neisseria.J Infect Dis. 1978 Sep;138(3):359-68. doi: 10.1093/infdis/138.3.359.
15	A non-sense mutation at Arg95 is predominant in complement 9 deficiency in Japanese.J Immunol. 1998 Feb 1;160(3):1509-13.