Meningitis

| Resident
Survival
Guide

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Template:DiseaseDisorder infobox

Meningitis Main Page

Patient Information

Overview

Causes

Classification

Viral Meningitis
Bacterial Meningitis
Fungal Meningitis

Differential Diagnosis

Diagnosis

Treatment

For patient information click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:  Niloofarsadaat Eshaghhosseiny, MD[2] Alara Ece Dagsali, M.D. Seyedmahdi Pahlavani, M.D. [3]
Synonyms and keywords: Leptomeningitis, Inflammation of meninges

## Overview

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The meninges (singular meninx) is the system of membranes which envelop the central nervous system. The meninges consist of three layers: the dura mater, the arachnoid mater, and the pia mater. The primary function of the meninges and of the cerebrospinal fluid is to protect the central nervous system. Meningitis is the inflammation of these protective membranes.
Meningitis may have been described in the Middle Ages, but it was first accurately identified by the Swiss Vieusseux (a scientific-literary association) during an outbreak in Geneva, Switzerland in 1805. In 1661, Thomas Willis first described the inflammation of meninges and an epidemic of meningitis. In the 17th century, Robert Whytt provided a detailed explanation of tuberculous meningitis and its stages. This was further elaborated by John Cheyne in the same century. Meningococcal meningitis was than described by Gaspard Vieusseux, Andre Matthey in Geneva and Elisa North in Massachussetes.
Meningitis may develop in response to a number of causes, including infectious agents (bacteria, viruses, fungi, or other organisms) or non-infectious causes, such as systemic illnesses that may involve CNS (e.g. neoplasms or connective tissue diseases, such as sarcoidosis, systemic lupus erythematosus (SLE), and wegener's) or certain drugs (e.g. nonsteroidal antiinflammatory drugs, intravenous immunoglobulin, intrathecal agents, and trimethoprim-sulfamethoxazole). While some forms of meningitis are mild and resolve spontaneously (e.g. viral meningitis), meningitis is a potentially serious condition owing to the proximity of the inflammation to the brain and spinal cord. The potential for serious neurologic damage or even death necessitates prompt medical attention and evaluation. The common presenting features of meningitis are, fever, neck stiffness and headache. Other symptoms include, photophobia (inability to tolerate bright light), phonophobia (inability to tolerate loud noises), irritability, altered mental status (in small children), and seizure. Physical examination of meningitis may vary in adults and infants. In adults, physical examination findings may include bradycardia, disorientation, papilledema, neck stiffness, positive brudzinski's and kernig's sign. However, petechial rash, bulging fontanelle, neck stiffness, jaundice, and convulsions are physical examination findings in infants. Diagnosis is based on clinical findings and CSF analysis. Treatment options are based on etiology and varies from supportive care and observing the patient (viral meningitis) to antibiotic therapy for bacterial meningitis or chemotherapy and/or irradiation for neoplastic meningitis.[1][2][3][4][5][6][4][7][8]

## Epidemiology

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Bacterial meningitis can be community acquired or health care associated.

* The major causes of community-acquired bacterial meningitis in adults in developed countries are Streptococcus pneumoniae, Neisseria meningitidis, and, primarily in patients over 50 years of age or those who have deficiencies in cell-mediated immunity, Listeria monocytogenes

* The major causes of health care-associated ventriculitis and meningitis are different (usually staphylococci and aerobic gram-negative bacilli) and occur more commonly after neurosurgical procedures (eg, post-craniotomy, ventriculoperitoneal shunts, lumbar shunts, external ventricular drains or following head trauma such as basilar skull fracture with or without clinical evidence of leak of cerebrospinal fluid)

A more detailed discussion of the epidemiology of and risk factors for bacterial meningitis is presented elsewhere.

## Causes

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| Etiology  | Common causes  | Less common causes

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Bacterial  |

* Streptococcus pneumoniae
* Neisseria meningitis
* Hemophilus influenza
* Group B streptococcus
* Listeria monocytogenes

* Staphylococcus aureus
* Klebsiella
* Pseudomonas
* E. coli
* Kingella Kingae
* Mycobacterium tuberculosis
* Diphtheroids
* Propionibacterium acnes
* Serratia marcescens
* Salmonella species
* Brucella sp
* Nocardia
* Francisella tularensis
* Streptococcus suis
* Ehrlichia chaffeensis

Viral  |

* Enteroviruses
* Herpes simplex viruses 1 and 2
* Arboviruses

* Influenza virus
* Herpes zoster
* Human Herpes Virus 6
* Epstein barr virus (EBV)
* Lymphocytic choriomeningitis virus
* Mumps
* Cytomegalo virus (CMV)
* Human immunodeficiency virus (HIV)
* West nile virus
* Human T cell lymphotrophic virus I and II
* Varicella zoster virus
* SARS-CoV-2 virus (corona virus)

Fungal  |

* Cryptococcus neoformans
* Aspergillus sp.
* Blastomyces dermatitidis
* Coccidioides immitis
* Candida spp.
* Histoplasma capsulatum
* Sporothrix schencki

* Xylohypha (formerly Cladosporium) trichoides and other dark-walled (demateaceous) fungi such as Curvularia and Drechslera
* Mucor
* Arthrographis kalrae
* Pneumocystis jirovecii[9][10]
* Cryptococcus albidus[11]

* Alternaria spp[12]

* Rhodotorula spp [13]

* Acremonium spp.[14]

* Dreschlera spp[15]

* Malassezia spp[16]

* Scedosporium spp[17]

* Arthrographis spp[18]

* Blastoschizomyces[19][20]

* Paecilomyces[21][22]

* Aureobasidium[23]

* Clavispora[24]

* Ustilago[25]

* Exophiala (Wangiella)[26]

* Exserohilum[27]

Spirochetal  |

* Treponema pallidum
* Borrelia burgdoferi

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Protozoal and Helminthic  |

* Amebas (Naegleria, Acanthamoeba, and Balamuthia)

* Angiostrongylus cantonensis
* Gnathostoma species
* Baylisascaris procyonis
* Toxocara species
* Taenia solium

Noninfectious conditions  |

* Neoplastic
* Sarcoidosis
* Systemic lupus erythematosus
* Granulomatosis with polyangiitis (Wegener's)
* Behçet's disease

* Fabry disease
* Central nervous system vasculitis
* Vogt-Koyanagi-Harada disease
* Chemical or drug-induced meningitis
* Nonsteroidal antiinflammatory drugs
* Intravenous immunoglobulin
* Intrathecal agents
* Certain antibiotics (eg, trimethoprim-sulfamethoxazole)

## Classification

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Meningitis could be classified to two main groups based on etiology:

* Infectious
* Non-infectious

### Infectious meningitis

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Infectious meningitis may be classified as the following algorithm based on chronicity of symptoms.

| Infectious Meningitis

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| Viral|

| Bacterial|

| Fungal|

| Acute|

| Chronic|

| Recurrent|

| Acute|

| Subacute|

| Chronic|

| Recurrent|

### Non-infectious meningitis

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Systemic illnesses, such as malignancies and connective tissue diseases (e.g. sarcoidosis, SLE, and wegener's) may involve meninges in their course and present as chronic meningitis.

Certain drugs may cause meningeal irritation and resemble as meningitis including:

* Nonsteroidal antiinflammatory drugs (NSAIDs)
* Intravenous immunoglobulin
* Intrathecal agents
* Certain antibiotics (eg, trimethoprim-sulfamethoxazole)

## Differential diagnosis

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Diseases | Symptoms  | Physical Examination | Past medical history | Diagnostic tests | Other Findings

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Headache | ↓LOC | Motor weakness | Abnormal sensory | Motor Deficit | Sensory deficit | Speech difficulty | Gait abnormality | Cranial nerves | CT /MRI | CSF Findings | Gold standard test
Meningitis | \+  | \-  | \-  | \-  | \-  | \+  | \+  | \-  | \-  | History of fever and malaise | \-  | ↑ Leukocytes,

↑ Protein

↓ Glucose

| CSF analysis[28] | Fever, neck

rigidity

Encephalitis | \+  | \+  | +/-  | +/-  | \-  | \-  | \+  | +/-  | \+  | History of fever and malaise | \+  | ↑ Leukocytes, ↓ Glucose  | CSF PCR | Fever, seizures, focal neurologic abnormalities
Brain tumor[29] | \+  | \-  | \-  | \-  | \+  | \+  | \+  | \-  | \+  | Weight loss, fatigue | \+  | Cancer cells[30] | MRI  | Cachexia, gradual progression of symptoms
Hemorrhagic stroke | \+  | \+  | \+  | \+  | \+  | \+  | \+  | \+  | \-  | Hypertension | \+  | \-  | CT scan without contrast[31][32] | Neck stiffness
Subdural hemorrhage | \+  | \+  | \+  | \+  | \+  | \-  | \-  | \-  | \+  | Trauma, fall  | \+  | Xanthochromia[33] | CT scan without contrast[31][32] | Confusion, dizziness, nausea, vomiting
Neurosyphilis[34][35] | \+  | \-  | \+  | \+  | \+  | \+  | \-  | \+  | \-  | STIs  | \+  | ↑ Leukocytes and protein | CSF VDRL-specifc

CSF FTA-Ab -sensitive[36]

| Blindness, confusion, depression,

Abnormal gait

Complex or atypical migraine | \+  | \-  | \+  | \+  | \-  | \-  | \+  | \-  | \-  | Family history of migraine | \-  | \-  | Clinical assesment  | Presence of aura, nausea, vomiting
Hypertensive encephalopathy | \+  | \+  | \-  | \-  | \-  | \-  | \+  | \+  | \-  | Hypertension | \+  | \-  | Clinical assesment  | Delirium, cortical blindness, cerebral edema, seizure
Wernicke’s encephalopathy | \-  | \+  | \-  | \-  | \-  | \+  | \+  | \+  | \+  | History of alcohal abuse  | \-  | \-  | Clinical assesment and lab findings  | Ophthalmoplegia, confusion
CNS abscess | \+  | \+  | \-  | \-  | \+  | \+  | \+  | \-  | \-  | History of drug abuse, endocarditis, immunosupression | \+  | ↑ leukocytes, ↓ glucose and ↑ protien  | MRI is more sensitive and specific  | High grade fever, fatigue,nausea, vomiting
Drug toxicity | \-  | \+  | \-  | \+  | \+  | \+  | \-  | \+  | \-  | \-  | \-  | \-  | Drug screen test  | Lithium, Sedatives, phenytoin, carbamazepine
Conversion disorder | \+  | \+  | \+  | \+  | \+  | \+  | \+  | \+  |  | History of emotional stress | \-  | \-  | Diagnosis of exclusion  | Tremors, blindness, difficulty swallowing
Metabolic disturbances (electrolyte imbalance, hypoglycemia)  | \-  | \+  | \+  | \+  | \+  | \+  | \-  | \-  | \+  | \-  | \-  | Hypoglycemia, hypo and hypernatremia, hypo and hyperkalemia | Depends on the cause  | Confusion, seizure, palpitations, sweating, dizziness, hypoglycemia
Multiple sclerosis exacerbation  | \-  | \-  | \+  | \+  | \-  | \+  | \+  | \+  | \+  | History of relapses and remissions  | \+  | ↑ CSF IgG levels

(monoclonal bands)

| Clinical assesment and MRI [37] | Blurry vision, urinary incontinence, fatigue
Seizure | \+  | \+  | \-  | \-  | \+  | \+  | \-  | \-  | \+  | Previous history of seizures | \-  | Mass lesion  | Clinical assesment and EEG [38] | Confusion, apathy, irritability,

## Diagnosis

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Diagnosis of meningitis, is based on clinical presentation in combination with CSF analysis. CSF analysis has major role for diagnosis and rule out other possibilities. The following table summarizes the CSF findings in different types of meningitis.[39][40][41][42][3]

Cerebrospinal fluid level | Normal level | Bacterial meningitis[42] | Viral meningitis (except SARS-CoV-2 meningitis) [42] | SARS-CoV-2 associated meningitis | Fungal meningitis | Tuberculous meningitis[43] | Neoplastic meningitis[39]

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Cells/ul | < 5 | >300 | 10-1000 | 10-1000 | 10-500 | 50-500 | >4
Cells | Lymphocyte | Leukocyte > Lymphocyte | Lymphocyte > Leukocyte | Lymphocyte > Neutrophil | Lymphocyte > Leukocyte | Lymphocyte > Leukocyte | Lymphocyte > Leukocyte
Total protein (mg/dl)  | 45-60 | Typically 100-500 | Normal or slightly high | Normal or slightly high | High | Typically 100-200 | >50
Glucose ratio (CSF/plasma)[40] | > 0.5 | < 0.3 | > 0.6 | > 0.6 | <0.3 | < 0.5 | <0.5
Lactate (mmols/l)[41] | < 2.1 | > 2.1 | < 2.1 | NA | >3.2 | > 2.1 | >2.1
Others | Intra-cranial pressure (ICP) = 6-12 (cm H2O) | CSF gram stain, CSF culture, CSF bacterial antigen | PCR of HSV-DNA, VZV | RT-PCR for detection of viral RNA i n CSF ( not approved by FDA) | CSF gram stain, CSF india ink | PCR of TB-DNA | CSF tumour markers such as alpha fetoprotein, CEA

## Treatment

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### Medical Therapy

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* Empiric therapy for meningitis must be initiated after CSF obtained.
* The choice of empiric antibiotic therapy is depend on patient age and underlying comorbid disease.
* Adapted from IDSA guidlines.

Predisposing factor | Common bacterial pathogen | Antimicrobial therapy

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1 month | Streptococcus agalactiae, Escherichia coli, Listeriamonocytogenes, Klebsiellaspecie | Ampicillin plus cefotaxime or ampicillin plus anaminoglycoside
1–23 months | Streptococcus pneumoniae, Neisseria meningitidis,S. agalactiae, Haemophilus influenzae, E. coli | Ampicillin plus cefotaxime or ampicillin plus anaminoglycoside
2–50 years,150 years | N . meningitidis, S. pneumoniae,S. pneumoniae, N. meningitidis, L. monocytogenes,aerobic gram-negative bacill | Vancomycin plus a third-generation cephalosporin,Vancomycin plus ampicillin plus a third-generationcephalosporina,
Head traumaBasilar skull fracture | S. pneumoniae, H. influenzae,group Ab-hemolyticstreptococci | Vancomycin plus a third-generation cephalospori
Penetrating trauma | Staphylococcus aureus,coagulase-negative staphylo-cocci (especiallyStaphylococcus epidermidis),aer-obic gram-negative bacilli (includingPseudomonasaeruginosa) | Vancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem
Postneurosurgery | Aerobic gram-negative bacilli (includingP. aeruginosa),S . aureus, coagulase-negative staphylococci (es-peciallyS. epidermidis) | ancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem
CSF shunt | Coagulase-negative staphylococci (especiallyS. epi-dermidis), S. aureus,aerobic gram-negative bacilli(includingP. aeruginosa), Propionibacterium acnes | ancomycin plus cefepime, vancomycin plus ceftazi-dime, or vancomycin plus meropenem

* Recommendations for antimicrobial therapy in adult patients with presumptive pathogen identification by positive Gram stain.
* Adapted from IDSA guidlines.

Microorganism | Recommended therapy | Alternative therapies | Duration oftherapy, days

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Streptococcus pneumoniae | Vancomycin plus a third-generationcephalosporina, | Meropenem , fluoroquinolonec | 7
Neisseria meningitidis | Third-generation cephalospori | Penicillin G, ampicillin, chloramphenicol, fluoro-quinolone, aztreonam | 7
Listeria monocytogenes | Ampicillindor penicillin G | Trimethoprim-sulfamethoxazole, meropenem | 10-14
Streptococcus agalactiae | Ampicillindor penicillin G | Third-generation cephalosporin | 14-21
Haemophilus influenzae | Third-generation cephalospori | Chloramphenicol, cefepime , meropenem ,fluoroquinolon | 21
Escherichia coli | Third-generation cephalospori | Cefepime, meropenem, aztreonam, fluoroquino-lone, trimethoprim-sulfamethoxazole | >21

### Surgery

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* Surgical intervention is not recommended for the management of meningitis.

### Primary Prevention

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* Adapted from the recommendations of the United States Centers for Disease Control and Prevention's (CDC's) Advisory Committee on Immunization Practices (ACIP) for the use of meningococcal vaccines.

Targeted group by age and/or risk factor | Primary dose(s) | Booster dose(s)

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For ages 11 through 18 years | Give one dose of Menactra or Menveo, preferably at age 11 or 12 years.

Discuss serogroup B meningococcus vaccination (Trumenba or Bexsero)*, which may be administered to adolescents and young adults 16 through 23 years of age; the preferred age for vaccination is 16 through 18 years of age (perhaps at the time of Menactra or Menveo booster).

| If primary dose was given at age ≤12 years, give Menactra or Menveo booster at age 16 years. If primary dose was given at age 13 to 15 years, give Menactra or Menveo booster at age 16 to 18 years
For individuals ages 19 through 21 years who are first year college students living in residence halls | If not yet received a dose of vaccine, give one dose of Menactra or Menveo.

Discuss serogroup B meningococcus vaccination (Trumenba or Bexsero)*, which may be administered to adolescents and young adults 16 through 23 years of age; the preferred age for vaccination is 16 through 18 years of age.

| Give Menactra or Menveo booster if previous dose given at age younger than 16 years.
|Patients with HIV infection
For age <2 years | Give four doses of Menveo (at ages 2, 4, 6, and 12 to 15 months) or give two doses of MenactraΔ (at age 9 to 23 months, 12 weeks apart). | Give additional dose of Menveo or Menactra three years after primary series. Booster doses should be repeated every five years thereafter.
For age ≥2 years | Give two doses of Menveo or Menactra 8 to 12 weeks apart. | For individuals age <7 years at previous dose, give additional dose of Menveo or Menactra three years after primary series. If the most recent dose was received before age 7 years, a booster dose should be readministered three years later. Booster doses should be repeated every five years thereafter.

For individuals age ≥7 years at previous dose, give additional dose of Menveo or Menactra five years after primary series; booster doses should be repeated every five years thereafter

Travelers to or residents of countries where meningococcal disease is hyperendemic or epidemic
For age 2 months through 18 months | Give Menveo at ages 2, 4, 6, and 12 to 15 months | If risk continues, give initial booster after three years followed by boosters every five years.
For children age 7 months through 23 months who have not initiated a series of Menveo | Give Menveo (if age 7 to 23 months)§ or Menactra (if age 9 to 23 months); administer two doses separated by three months | If risk continues, give initial booster after three years followed by boosters every five years.
For age 2 years through 55 years | Give one dose of Menactra or Menveo. | Boost every five years with Menactra or Menveo
For age 56 years and older | Give one dose of Menactra or Menveo | Boost every five years with Menactra or Menveo
People with prolonged increased risk for exposure (eg, military recruits, microbiologists routinely working with Neisseria meningitidis)
For age 10 years and older | Give one dose of Menactra or Menveo.

Give either Trumenba (three doses administered at 0, 1 to 2, and 6 months) or Bexsero (two doses administered at least one month apart)

| Boost every five years with Menactra or Menveo.

Boost with one dose MenB (Trumenba or Bexsero) one year after primary series; revaccinate every 2 to 3 years if risk remains.

People present during outbreaks caused by a meningococcal vaccine serogroup
For age 2 months through 18 months | Give Menveo at ages 2, 4, 6, and 12 to 15 months. | '
For children age 7 months through 23 months who have not initiated a series of Menveo | Give Menveo (if age 7 to 23 months)§ or Menactra (if age 9 to 23 months); administer two doses separated by 3 months | '
For age 2 years through 9 years | Give one dose of Menactra or Menveo | '
For age 10 years through 55 years | Give one dose of Menactra or Menveo.

Give either Trumenba (three doses administered at 0, 1 to 2, and 6 months) or Bexsero (two doses administered at least one month apart)

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For age 56 years and older | Give one dose of Menactra or Menveo.

Give either Trumenba (three doses administered at 0, 1 to 2, and 6 months) or Bexsero (two doses administered at least one month apart)

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People with persistent complement component deficiencies
For age 2 months through 18 months | Give Menveo at ages 2, 4, 6, and 12 to 15 months. | Give Menactra or Menveo booster after three years followed by boosters every five years thereafter.
For children age 7 months through 23 months who have not initiated a series of Menveo | Give Menveo (if age 7 to 23 months)§ or Menactra (if age 9 to 23 months); administer two doses separated by three months. | '
For age 2 years through 9 years | Give two doses of Menactra or Menveo two months apart. | Boost every five years with Menactra or Menveo
For age 10 years through 55 years | ive two doses of Menactra or Menveo two months apart and either Trumenba (three doses administered at 0, 1 to 2, and 6 months) or Bexsero (two doses administered at least one month apart) | Boost every five years with Menactra or Menveo.

Boost with one dose MenB (Trumenba or Bexsero) one year after primary series; revaccinate every 2 to 3 years if risk remains.

For age 56 years and older | Give two doses of Menactra or Menveo two months apart and either Trumenba (three doses administered at 0, 1 to 2, and 6 months) or Bexsero (two doses administered at least one month apart) | Boost every five years with Menactra or Menveo.

Boost with one dose MenB (Trumenba or Bexsero) one year after primary series; revaccinate every 2 to 3 years if risk remains.

People with functional or anatomic asplenia, including sickle cell disease
For age 2 months through 18 months | Give Menveo at ages 2, 4, 6, and 12 months. | Give Menactra or Menveo booster after three years followed by boosters every five years thereafter.
For children age 19 months through 23 months who have not initiated a series of Menveo | Give two doses of Menveo three months apart. | Give Menactra or Menveo booster after three years followed by boosters every five years thereafter.
For age 2 years through 9 years | Give two doses of Menactra or Menveo two months apart | Boost every five years with Menactra or Menveo
For age 10 years through 55 years | Give two doses of Menactra or Menveo two months apart and either Trumenba (three doses administered at 0, 1 to 2, and 6 months) or Bexsero (two doses administered at least one month apart) | Boost every five years with Menactra or Menveo.

Boost with one dose MenB (Trumenba or Bexsero) one year after primary series; revaccinate every 2 to 3 years if risk remains

For age 56 years and older | Give two doses of Menactra or Menveo two months apart and either Trumenba (three doses administered at 0, 1 to 2, and 6 months) or Bexsero (two doses administered at least one month apart). | Boost every five years with Menactra or Menveo.

Boost with one dose MenB (Trumenba or Bexsero) one year after primary series; revaccinate every 2 to 3 years if risk remains.

The quadrivalent meningococcal conjugate vaccines (MenACWY) are Menactra (MenACWY-DT) and Menveo (MenACWY-CRM); these have replaced the quadrivalent meningococcal polysaccharide vaccine Menomune (MPSV4). MenHibrix (HibMenCY), a combination conjugate vaccine against meningococcus serogroups C and Y and Haemophilus influenzae type b, was discontinued in 2017. Trumenba (MenB-FHbp) and Bexsero (MenB-4C) are meningococcus serogroup B vaccines.

### Secondary Prevention

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* Secondary prevention with Antimicrobial chemoprophylaxis is necessary for individuals who have close contact with patients with invasive meningococcal disease. Close contacts include:
* 1.household members , 2.child-care center contacts ,3.anyone directly exposed to the patient's oral secretions (e.g., through kissing, mouth-to-mouth resuscitation, endotracheal intubation, or endotracheal tube management) in the 7 days before symptom onset. Health-care personnel should receive chemoprophylaxis if they were managing an airway or exposed to respiratory secretions of a patient with meningococcal disease. For travelers, antimicrobial chemoprophylaxis should be considered for any passenger who had direct contact with respiratory secretions from an index-patient or for anyone seated directly next to an index-patient on a prolonged flight (i.e., one lasting ≥8 hours)

* Recommended chemoprophylaxis regimens for protection against meningococcal disease — Advisory Committee on Immunization Practices (ACIP), United States, 2012

Drug | Age group | Dosage | Duration and route of administration

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Rifampin | Children aged <1 mo | 5 mg/kg every 12 hrs | 2 days
Rifampin | Children aged ≥1 mo | 10 mg/kg every 12 hrs | 2 days
Rifampin | Adults | 600 mg every 12 hrs | 2 days
Ciprofloxacin | Adults | 500 mg | Single dose
Ceftriaxone | Children age <15 yrs | 125 mg | Single IM dose
Ceftriaxone | Adults | 250 mg | Single IM dose

## References

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1. ↑ Attia J, Hatala R, Cook DJ, Wong JG (1999). "The rational clinical examination. Does this adult patient have acute meningitis?". JAMA. 282 (2): 175–81. PMID 10411200.CS1 maint: Multiple names: authors list (link)
2. ↑ https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0047163/ Accessed on Jan 9th, 2017
3. ↑ 3.0 3.1 Brouwer MC, Tunkel AR, van de Beek D (2010). "Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis". Clin Microbiol Rev. 23 (3): 467–92. doi:10.1128/CMR.00070-09. PMC 2901656. PMID 20610819.CS1 maint: Multiple names: authors list (link)
4. ↑ 4.0 4.1 Durand ML, Calderwood SB, Weber DJ, Miller SI, Southwick FS, Caviness VS; et al. (1993). "Acute bacterial meningitis in adults. A review of 493 episodes". N Engl J Med. 328 (1): 21–8. doi:10.1056/NEJM199301073280104. PMID 8416268.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
5. ↑ van de Beek D, de Gans J, Spanjaard L, Weisfelt M, Reitsma JB, Vermeulen M (2004). "Clinical features and prognostic factors in adults with bacterial meningitis". N Engl J Med. 351 (18): 1849–59. doi:10.1056/NEJMoa040845. PMID 15509818.CS1 maint: Multiple names: authors list (link)
6. ↑ van de Beek D, de Gans J, Spanjaard L, Weisfelt M, Reitsma JB, Vermeulen M (2004). "Clinical features and prognostic factors in adults with bacterial meningitis". N. Engl. J. Med. 351 (18): 1849–59. doi:10.1056/NEJMoa040845. PMID 15509818.CS1 maint: Multiple names: authors list (link)
7. ↑ Domingo P, Mancebo J, Blanch L, Net A, Nolla J (1988). "Fever in adult patients with acute bacterial meningitis". J Infect Dis. 158 (2): 496. PMID 3403999.CS1 maint: Multiple names: authors list (link)
8. ↑ Thomas KE, Hasbun R, Jekel J, Quagliarello VJ (2002). "The diagnostic accuracy of Kernig's sign, Brudzinski's sign, and nuchal rigidity in adults with suspected meningitis". Clin Infect Dis. 35 (1): 46–52. doi:10.1086/340979. PMID 12060874.CS1 maint: Multiple names: authors list (link)
9. ↑ Villanueva JL, Cordero E, Caballero-Granado FJ, Regordan C, Becerril B, Pachón J (1997). "Pneumocystis carinii meningoradiculitis in a patient with AIDS". Eur J Clin Microbiol Infect Dis. 16 (12): 940–2. PMID 9495679.CS1 maint: Multiple names: authors list (link)
10. ↑ Baena Luna MR, Muñoz García J, Grancha Bertolín L, Sanz García M (1998). "[Presence of Pneumocystis carinii in cerebrospinal fluid]". An Med Interna. 15 (5): 265–6. PMID 9629775.CS1 maint: Multiple names: authors list (link)
11. ↑ Melo JC, Srinivasan S, Scott ML, Raff MJ (1980). "Cryptococcus albidus meningitis". J Infect. 2 (1): 79–82. PMID 7185917.CS1 maint: Multiple names: authors list (link)
12. ↑ OHASHI Y (1960). "On a rare disease due to Alternaria tenuis Nees (alternariasis)". Tohoku J Exp Med. 72: 78–82. PMID 13730495.
13. ↑ Shinde RS, Mantur BG, Patil G, Parande MV, Parande AM (2008). "Meningitis due to Rhodotorula glutinis in an HIV infected patient". Indian J Med Microbiol. 26 (4): 375–7. PMID 18974495.CS1 maint: Multiple names: authors list (link)
14. ↑ Fincher RM, Fisher JF, Lovell RD, Newman CL, Espinel-Ingroff A, Shadomy HJ (1991). "Infection due to the fungus Acremonium (cephalosporium)". Medicine (Baltimore). 70 (6): 398–409. PMID 1956281.CS1 maint: Multiple names: authors list (link)
15. ↑ Fuste FJ, Ajello L, Threlkeld R, Henry JE (1973). "Drechslera hawaiiensis: causative agent of a fatal fungal meningo-encephalitis". Sabouraudia. 11 (1): 59–63. PMID 4739938.CS1 maint: Multiple names: authors list (link)
16. ↑ Rosales CM, Jackson MA, Zwick D (2004). "Malassezia furfur meningitis associated with total parenteral nutrition subdural effusion". Pediatr Dev Pathol. 7 (1): 86–90. doi:10.1007/s10024-003-4030-5. PMID 15255040.CS1 maint: Multiple names: authors list (link)
17. ↑ Symoens F, Knoop C, Schrooyen M, Denis O, Estenne M, Nolard N; et al. (2006). "Disseminated Scedosporium apiospermum infection in a cystic fibrosis patient after double-lung transplantation". J Heart Lung Transplant. 25 (5): 603–7. doi:10.1016/j.healun.2005.12.011. PMID 16678041.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
18. ↑ Chin-Hong PV, Sutton DA, Roemer M, Jacobson MA, Aberg JA (2001). "Invasive fungal sinusitis and meningitis due to Arthrographis kalrae in a patient with AIDS". J Clin Microbiol. 39 (2): 804–7. doi:10.1128/JCM.39.2.804-807.2001. PMC 87827. PMID 11158158.CS1 maint: Multiple names: authors list (link)
19. ↑ Girmenia C, Micozzi A, Venditti M, Meloni G, Iori AP, Bastianello S; et al. (1991). "Fluconazole treatment of Blastoschizomyces capitatus meningitis in an allogeneic bone marrow recipient". Eur J Clin Microbiol Infect Dis. 10 (9): 752–6. PMID 1810730.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
20. ↑ Naficy AB, Murray HW (1990). "Isolated meningitis caused by Blastoschizomyces capitatus". J Infect Dis. 161 (5): 1041–2. PMID 2324536.
21. ↑ Kantarcioğlu AS, Hatemi G, Yücel A, De Hoog GS, Mandel NM (2003). "Paecilomyces variotii central nervous system infection in a patient with cancer". Mycoses. 46 (1–2): 45–50. PMID 12588483.CS1 maint: Multiple names: authors list (link)
22. ↑ Fagerburg R, Suh B, Buckley HR, Lorber B, Karian J (1981). "Cerebrospinal fluid shunt colonization and obstruction by Paecilomyces variotii. Case report". J Neurosurg. 54 (2): 257–60. doi:10.3171/jns.1981.54.2.0257. PMID 7192726.CS1 maint: Multiple names: authors list (link)
23. ↑ Kutleša M, Mlinarić-Missoni E, Hatvani L, Voncina D, Simon S, Lepur D; et al. (2012). "Chronic fungal meningitis caused by Aureobasidium proteae". Diagn Microbiol Infect Dis. 73 (3): 271–2. doi:10.1016/j.diagmicrobio.2012.03.007. PMID 22504065.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
24. ↑ Krcmery V, Mateicka F, Grausova S, Kunova A, Hanzen J (1999). "Invasive infections due to Clavispora lusitaniae". FEMS Immunol Med Microbiol. 23 (1): 75–8. PMID 10030550.CS1 maint: Multiple names: authors list (link)
25. ↑ MOORE M, RUSSELL WO, SACHS E (1946). "Chronic leptomeningitis and ependymitis caused by Ustilago, probably U. zeae (corn smut)". Am J Pathol. 22: 761–77. PMID 20991975.CS1 maint: Multiple names: authors list (link)
26. ↑ Centers for Disease Control and Prevention (CDC) (2002). "Exophiala infection from contaminated injectable steroids prepared by a compounding pharmacy--United States, July-November 2002". MMWR Morb Mortal Wkly Rep. 51 (49): 1109–12. PMID 12530707.
27. ↑ Pettit AC, Pugh ME (2013). "Index case for the fungal meningitis outbreak, United States". N Engl J Med. 368 (10): 970. doi:10.1056/NEJMc1300630. PMID 23465119.
28. ↑ Carbonnelle E (2009). "[Laboratory diagnosis of bacterial meningitis: usefulness of various tests for the determination of the etiological agent]". Med Mal Infect. 39 (7–8): 581–605. doi:10.1016/j.medmal.2009.02.017. PMID 19398286.
29. ↑ Morgenstern LB, Frankowski RF (1999). "Brain tumor masquerading as stroke". J Neurooncol. 44 (1): 47–52. PMID 10582668.
30. ↑ Weston CL, Glantz MJ, Connor JR (2011). "Detection of cancer cells in the cerebrospinal fluid: current methods and future directions". Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.CS1 maint: Multiple names: authors list (link)
31. ↑ 31.0 31.1 Birenbaum D, Bancroft LW, Felsberg GJ (2011). "Imaging in acute stroke". West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.CS1 maint: Multiple names: authors list (link)
32. ↑ 32.0 32.1 DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). "ACR Appropriateness Criteria® on cerebrovascular disease". J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
33. ↑ Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). "Cerebrospinal fluid in cerebral hemorrhage and infarction". Stroke. 6 (6): 638–41. PMID 1198628.CS1 maint: Multiple names: authors list (link)
34. ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). "Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients". J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
35. ↑ Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
36. ↑ Ho EL, Marra CM (2012). "Treponemal tests for neurosyphilis--less accurate than what we thought?". Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
37. ↑ Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). "Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group". Arch Neurol. 51 (1): 61–6. PMID 8274111.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
38. ↑ Manford M (2001). "Assessment and investigation of possible epileptic seizures". J Neurol Neurosurg Psychiatry. 70 Suppl 2: II3–8. PMC 1765557. PMID 11385043.
39. ↑ 39.0 39.1 Le Rhun E, Taillibert S, Chamberlain MC (2013). "Carcinomatous meningitis: Leptomeningeal metastases in solid tumors". Surg Neurol Int. 4 (Suppl 4): S265–88. doi:10.4103/2152-7806.111304. PMC 3656567. PMID 23717798.CS1 maint: Multiple names: authors list (link)
40. ↑ 40.0 40.1 Chow E, Troy SB (2014). "The differential diagnosis of hypoglycorrhachia in adult patients". Am J Med Sci. 348 (3): 186–90. doi:10.1097/MAJ.0000000000000217. PMC 4065645. PMID 24326618.
41. ↑ 41.0 41.1 Leen WG, Willemsen MA, Wevers RA, Verbeek MM (2012). "Cerebrospinal fluid glucose and lactate: age-specific reference values and implications for clinical practice". PLoS One. 7 (8): e42745. doi:10.1371/journal.pone.0042745. PMC 3412827. PMID 22880096.CS1 maint: Multiple names: authors list (link)
42. ↑ 42.0 42.1 42.2 Negrini B, Kelleher KJ, Wald ER (2000). "Cerebrospinal fluid findings in aseptic versus bacterial meningitis". Pediatrics. 105 (2): 316–9. PMID 10654948.CS1 maint: Multiple names: authors list (link)
43. ↑ Caudie C, Tholance Y, Quadrio I, Peysson S (2010). "[Contribution of CSF analysis to diagnosis and follow-up of tuberculous meningitis]". Ann Biol Clin (Paris). 68 (1): 107–11. doi:10.1684/abc.2010.0407. PMID 20146981.CS1 maint: Multiple names: authors list (link)

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