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Meningitis

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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

Overview

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

Epidemiology

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

Causes


Etiology Common causes Less common causes
Bacterial
Viral
Fungal
  • Arthrographis spp[18]
Spirochetal —
Protozoal and Helminthic
Noninfectious conditions


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Mugilan Poongkunran M.B.B.S [3]

Overview

Most cases of meningitis are caused by microorganisms, such as viruses, bacteria, fungi, or parasite, that spread through blood and into the cerebrospinal fluid (CSF).[1] Non-infectious causes include cancer, systemic lupus erythematosus and certain drugs. The most common cause of meningitis is viral, and often runs its course within a few days. Bacterial meningitis is the second most frequent type and can be serious and life-threatening. Numerous microorganisms may cause bacterial meningitis, but Neisseria meningitidis and Streptococcus pneumoniae are the most common pathogens in patients without immune deficiency, with meningococcal disease being more common in children. Staphylococcus aureus may complicate neurosurgical operations, and Listeria monocytogenes is associated with poor nutritional state and alcoholicism. Haemophilus influenzae (type B) incidence has been much reduced by immunization in many countries. Mycobacterium tuberculosis (the causative agent of tuberculosis) rarely causes meningitis in Western countries but is common and feared in countries where tuberculosis is endemic.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ System

Cardiovascular No underlying causes
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic Vogt-Koyanagi-Harada syndrome
Drug Side Effect Allopurinol, amoxicillin, antiepileptic drugs, azathioprine, cetuximab, ibuprofen, intravenous immunoglobulin, isoniazid, lamotrigine, methotrexate, NSAIDs, Oxaprozin, Pergolide, phenazopyridine, rofecoxib, Sulfasalazine, trimethoprim-sulfamethoxazole, Ziconotide
Ear Nose Throat Cholesteatoma, otitis media, sinusitis
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic Whipple’s disease
Genetic Common variable immunodeficiency, X-linked agammaglobulinemia
Hematologic Kikuchi disease, X-linked agammaglobulinemia
Iatrogenic Transsphenoidal surgery
Infectious Disease Acanthamoeba, Actinomyces, Acinetobacter, adenovirus, Angiostrongylus cantonensis, anthrax, arboviruses, Aspergillus, bacteremia, Bacteroides, Bartonellosis, Blastomyces dermatitidis, Borrelia burgdorferi, Brucella, Burkholderia pseudomallei, California encephalitis virus, campylobacter, candida, Chagas disease, chicken pox, Chlamydia, Citrobacter koseri, coagulase-negative staphylococci, Coccidioides immitis, Colorado tick fever, coxsackie A virus, coxsackie B virus, Cryptococcus neoforman, cytomegalovirus, eastern equine encephalitis virus, echovirus, Ehrlichiosis, enteroviruses, epidural abscess, Epstein Barr virus, Escherichia coli, flavivirus, gram-negative bacilli, Haemophilus influenzae, herpes simplex type II, herpes simplex type I, Histoplasma capsulatum, human immunodeficiency virus, influenza virus, Klebsiella, Leptospira, Listeria monocytogenes, Lyme disease, lymphocytic choriomeningitis virus, malaria, measles, mumps virus, Mycobacterium avium-intracellulare, Mycoplasma hominis, Mycoplasma pneumoniae, Naegleria fowleri, neisseria meningitidis, Nocardia, Non-Group B streptococci, otitis media, parainfluenza, Pasteurella multocida, Pasteurella stomatis, poliovirus, Powassan encephalitis, Pseudomonas aeruginosa, rabies virus, Rat-bite fever, relapsing fever, Rickettsia, rocky mountain spotted fever, roseola, rotavirus, rubella, Salmonella, Schistosomiasis, Serratia, Serratia marcescens, simian herpes B virus, sinusitis, Sporothrix schenckii, St. Louis encephalitis virus, Staphylococcus aureus, Streptococcus agalactiae, Streptococcus pneumoniae, Streptococcus suis, subdural abscess, syphilis, Toxoplasma gondii, Treponema pallidum, Trichinosis, Trypanosomiasis, tuberculous meningitis, typhoid fever, varicella zoster virus, Venezuelan equine encephalitis virus, west nile virus, western equine encephalitis virus, Yersinia pestis
Musculoskeletal/Orthopedic No underlying causes
Neurologic Epidural abscess, leptomeningeal metastasis, meningeal carcinomatosis, subdural abscess
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Leptomeningeal metastasis, meningeal carcinomatosis
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy Behcet’s disease, complement deficiency, Kawasaki disease, sarcoidosis, systemic lupus erythematosus
Sexual No underlying causes
Trauma Head injury, skull fracture
Urologic No underlying causes
Miscellaneous Post-vaccination

Causes in Alphabetical Order


References

  1. ↑ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. 876&ndash, 9. ISBN 0838585299.
  2. ↑ Chi M, Kim HJ, Haug S, Vagefi R, Kersten RC (2014). “Acute eosinophilic meningitis and orbital inflammation from presumed angiostrongyliasis”. Can J Ophthalmol. 49 (3): e65–7. doi:10.1016/j.jcjo.2014.02.011. PMID 24862785.
  3. ↑ Maniyar F, Rooney C, Lily O, Bazaz R (2009). “Anticonvulsant hypersensitivity syndrome presenting as aseptic meningitis”. J Neurol. 256 (7): 1190–1. doi:10.1007/s00415-009-5089-3. PMID 19330481.
  4. ↑ Starkey J, Moritani T, Kirby P (2014). “MRI of CNS Fungal Infections: Review of Aspergillosis to Histoplasmosis and Everything in Between”. Clin Neuroradiol. doi:10.1007/s00062-014-0305-7. PMID 24870817.
  5. ↑ Feinstein TM, Gibson MK, Argiris A (2009). “Cetuximab-induced aseptic meningitis”. Ann Oncol. 20 (9): 1609–10. doi:10.1093/annonc/mdp382. PMID 19643807.
  6. ↑ Rodrigues J, Rocha D, Santos F, João A (2014). “Neonatal Citrobacter koseri Meningitis: Report of Four Cases”. Case Rep Pediatr. 2014: 195204. doi:10.1155/2014/195204. PMC 3971854. PMID 24716069.
  7. ↑ Sloan DJ, Parris V (2014). “Cryptococcal meningitis: epidemiology and therapeutic options”. Clin Epidemiol. 6: 169–182. doi:10.2147/CLEP.S38850. PMC 4026566. PMID 24872723.
  8. ↑ Neal JW (2014). “Flaviviruses are neurotropic , but how do they invade the CNS ?”. J Infect. doi:10.1016/j.jinf.2014.05.010. PMID 24880028.
  9. ↑ Jolles S, Sewell WA, Leighton C (2000). “Drug-induced aseptic meningitis: diagnosis and management”. Drug Saf. 22 (3): 215–26. PMID 10738845.
  10. ↑ Agnihotri SP, Wuthrich C, Dang X, Nauen D, Karimi R, Viscidi R; et al. (2014). “A fatal case of JC virus meningitis presenting with hydrocephalus in an HIV-seronegative patient”. Ann Neurol. doi:10.1002/ana.24192. PMID 24895208.
  11. ↑ Khishfe BF, Krass LM, Nordquist EK (2014). “Kikuchi disease presenting with aseptic meningitis”. Am J Emerg Med. doi:10.1016/j.ajem.2014.03.029. PMID 24746858.
  12. ↑ Almeida SM, Nogueira Kda S, Palmeiro JK, Scheffer MC, Stier CJ, França JC; et al. (2014). “Nosocomial meningitis caused by Klebsiella pneumoniae producing carbapenemase, with initial cerebrospinal fluid minimal inflammatory response”. Arq Neuropsiquiatr. 72 (5): 398–9. PMID 24863522.
  13. ↑ Simms KM, Kortepeter C, Avigan M (2012). “Lamotrigine and aseptic meningitis”. Neurology. 78 (12): 921–7. doi:10.1212/WNL.0b013e31824c4634. PMID 22357718.
  14. ↑ Chamberlain M, Soffietti R, Raizer J, Rudà R, Brandsma D, Boogerd W; et al. (2014). “Leptomeningeal metastasis: a Response Assessment in Neuro-Oncology critical review of endpoints and response criteria of published randomized clinical trials”. Neuro Oncol. doi:10.1093/neuonc/nou089. PMID 24867803.
  15. ↑ Hoppmann RA, Peden JG, Ober SK (1991). “Central nervous system side effects of nonsteroidal anti-inflammatory drugs. Aseptic meningitis, psychosis, and cognitive dysfunction”. Arch Intern Med. 151 (7): 1309–13. PMID 2064481.
  16. ↑ Foguem C (2014). “Rare Case of Catastrophic Diffuse Hemorrhage Complicating Sepsis and Meningitis Due to Pasteurella stomatis in an Elderly Woman Mimicking Hemorrhagic Septicemia”. J Am Med Dir Assoc. doi:10.1016/j.jamda.2014.04.008. PMID 24895000.
  17. ↑ Riedmann EM (2014). “Human vaccines & immunotherapeutics: news”. Hum Vaccin Immunother. 10 (1): 3–6. doi:10.4161/hv.28052. PMID 24832716.
  18. ↑ Schwartz KL, Richardson SE, Ward KN, Donaldson C, Macgregor D, Banwell B; et al. (2014). “Delayed Primary HHV-7 Infection and Neurologic Disease”. Pediatrics. doi:10.1542/peds.2013-3344. PMID 24819578.
  19. ↑ Lombardi D, Malaspina S, Strippoli A, Lucarelli C, Luzzi I, Ripabelli G (2014). “Salmonella enterica serovar Virchow meningitis in a young man in Italy: a case report”. J Med Case Rep. 8 (1): 139. doi:10.1186/1752-1947-8-139. PMC 4031895. PMID 24884674.
  20. ↑ Ersoz G, Uguz M, Aslan G, Horasan ES, Kaya A (2014). “Outbreak of meningitis due to Serratia marcescens after spinal anaesthesia”. J Hosp Infect. 87 (2): 122–5. doi:10.1016/j.jhin.2014.03.004. PMID 24814159.
  21. ↑ Gómez-Zorrilla S, Ardanuy C, Lora-Tamayo J, Cámara J, García-Somoza D, Peña C; et al. (2014). “Streptococcus suis Infection and Malignancy in Man, Spain”. Emerg Infect Dis. 20 (6). doi:10.3201/eid2006.131167. PMC 4036790. PMID 24856779.
  22. ↑ Yoon KW, Cho CS, Lee SK (2014). “Large intracranial aneurysm after transsphenoidal surgery for pituitary macroadenoma”. J Korean Neurosurg Soc. 55 (3): 160–3. doi:10.3340/jkns.2014.55.3.160. PMC 4024817. PMID 24851153.
  23. ↑ Escalante A, Stimmler MM (1992). “Trimethoprim-sulfamethoxasole induced meningitis in systemic lupus erythematosus”. J Rheumatol. 19 (5): 800–2. PMID 1613713.
  24. ↑ Van Vu Q, Wada T, Le HT, Le HT, Van Nguyen AT, Osamu O; et al. (2014). “Clinical and mutational features of Vietnamese children with X-linked agammaglobulinemia”. BMC Pediatr. 14 (1): 129. doi:10.1186/1471-2431-14-129. PMID 24885015.

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Classification

Classification

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

  • Infectious
  • Non-infectious

Infectious meningitis

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

 
 
 
 
 
 
 
 
 
 
 
 
 
 
Infectious Meningitis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Viral
 
 
 
 
 
 
 
Bacterial
 
 
 
 
 
 
 
 
 
 
 
 
Fungal
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Acute
 
Chronic
 
Recurrent
 
 
Acute
 
Subacute
 
Chronic
 
 
Recurrent


Non-infectious meningitis

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:

Differential diagnosis

Differential diagnosis

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


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Meningitis must be differentiated from brain abscess, encephalitis, brain tumor, subarachnoid hemorrhage, and delirium tremens. The rash component of meningitis must be differentiated from other diseases that cause skin rash, such as chickenpox, herpes zoster, erythema multiforme, and Kawasaki disease.

Differentiating Meningitis from other Diseases

  • Brain abscess – Brain abscess is a focal infection of the brain parenchyma commonly caused by bacteria, fungal and parasitic pathogens. Imaging and neurosurgical aspiration is required for differentiation in addition to CSF profile.
  • Encephalitis – Encephalitis is the inflammation of brain. Meningitis can itself cause encephalitis and is called meningoencephalitis. The symptoms appear gradually in encephalitis but occur abruptly in meningitis.
  • Delirium tremens – Delirium tremens and alcohol withdrawal should be differentiated from meningitis especially when present with confusion and fever. Both the conditions can coexist.
  • Brain tumor – Brain tumors can simulate purulent meningitis with symptoms of fever, signs of meningeal irritation and marked CSF pleocytosis. Irritation of leptomeninges by tumor and its breakdown products causes these symptoms.[1] Determination of creatine kinase BB and carcinoembryonic antigenhelps in differentiating.[2]
  • Subarachnoid hemorrhage – Subarachnoid hemorrhage also presents with severe headache, neck stiffness, nausea and vomiting like meningitis. It is a medical emergency. Imaging studies help in differentiation. Tubercular meningitis should be considered in the differential diagnosis in cases of nonaneurysmal subarachnoid hemorrhage.[3]

Rash Component

Different rash-like conditions can be confused with meningitis and are thus included in its differential diagnosis. The various conditions that should be differentiated from meningitis include:[4][5][6][7][8][9][10]

Disease Features
Impetigo 
  • It commonly presents with pimple-like lesions surrounded by erythematous skin. Lesions are pustules, filled with pus, which then break down over 4-6 days and form a thick crust. It’s often associated with insect bites, cuts, and other forms of trauma to the skin.
Insect bites
  • The insect injects formic acid, which can cause an immediate skin reaction often resulting in a rash and swelling in the injured area, often with formation of vesicles.
Kawasaki disease
Measles
Monkeypox
  • The presentation is similar to smallpox, although it is often a milder form, with fever, headache, myalgia, back pain, swollen lymph nodes, a general feeling of discomfort, and exhaustion. Within 1 to 3 days (sometimes longer) after the appearance of fever, the patient develops a papular rash, often first on the face. The lesions usually develop through several stages before crusting and falling off.
Rubella
Atypical measles
Coxsackievirus
  • The most commonly caused disease is the Coxsackie A disease, presenting as hand, foot and mouth disease. It may be asymptomatic or cause mild symptoms, or it may produce fever and painful blisters in the mouth (herpangina), on the palms and fingers of the hand, or on the soles of the feet. There can also be blisters in the throat or above the tonsils. Adults can also be affected. The rash, which can appear several days after high temperature and painful sore throat, can be itchy and painful, especially on the hands/fingers and bottom of feet.
Acne
Syphilis It commonly presents with gneralized systemic symptoms such as malaise, fatigue, headache and fever. Skin eruptions may be subtle and asymptomatic It is classically described as:
Molluscum contagiosum
  • The lesions are commonly flesh-colored, dome-shaped, and pearly in appearance. They are often 1-5 millimeters in diameter, with a dimpled center. Generally not painful, but they may itch or become irritated. Picking or scratching the lesions may lead to further infection or scarring. In about 10% of the cases, eczema develops around the lesions. They may occasionally be complicated by secondary bacterial infections.
Mononucleosis
Toxic erythema
  • It is a common rash in infants, with clustered and vesicular appearance.
Rat-bite fever
  • It commonly presents with fever, chills, open sore at the site of the bite and rash, which may show red or purple plaques.
Parvovirus B19
  • The rash of fifth disease is typically described as “slapped cheeks,” with erythema across the cheeks and sparing the nasolabial folds, forehead, and mouth.
Cytomegalovirus
Scarlet fever
Rocky Mountain spotted fever
Stevens-Johnson syndrome
  • The symptoms may include fever, sore throat and fatigue. Commonly presents ulcers and other lesions in the mucous membranes, almost always in the mouth and lips but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient’s ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children. A rash of round lesions about an inch across, may arise on the face, trunk, arms and legs, and soles of the feet, but usually not on the scalp.
Varicella-zoster virus
  • It commonly starts as a painful rash on one side of the face or body. The rash forms blisters that typically scab over in 7-10 days and clears up within 2-4 weeks.
Chickenpox
  • It commonly starts with conjunctival and catarrhal symptoms and then characteristic spots appearing in two or three waves, mainly on the body and head, rather than the hands, becoming itchy raw pox (small open sores which heal mostly without scarring). Touching the fluid from a chickenpox blister can also spread the disease.
Meningococcemia
Rickettsial pox
Meningitis

References

  1. ↑ Soffer D (1976) Brain tumors simulating purulent meningitis. Eur Neurol 14 (3):192-7. PMID: 1278192
  2. ↑ Terheggen HG (1985) [CNS tumors with the clinical picture of meningitis.] Monatsschr Kinderheilkd 133 (1):13-9. PMID: 3883130
  3. ↑ Yeh ST, Lee WJ, Lin HJ, Chen CY, Te AL, Lin HJ (2003) Nonaneurysmal subarachnoid hemorrhage secondary to tuberculous meningitis: report of two cases. J Emerg Med 25 (3):265-70. PMID: 14585453
  4. ↑ Hartman-Adams H, Banvard C, Juckett G (2014). “Impetigo: diagnosis and treatment”. Am Fam Physician. 90 (4): 229–35. PMID 25250996.
  5. ↑ Mehta N, Chen KK, Kroumpouzos G (2016). “Skin disease in pregnancy: The approach of the obstetric medicine physician”. Clin Dermatol. 34 (3): 320–6. doi:10.1016/j.clindermatol.2016.02.003. PMID 27265069.
  6. ↑ Moore, Zack S; Seward, Jane F; Lane, J Michael (2006). “Smallpox”. The Lancet. 367 (9508): 425–435. doi:10.1016/S0140-6736(06)68143-9. ISSN 0140-6736.
  7. ↑ Ibrahim F, Khan T, Pujalte GG (2015). “Bacterial Skin Infections”. Prim Care. 42 (4): 485–99. doi:10.1016/j.pop.2015.08.001. PMID 26612370.
  8. ↑ Ramoni S, Boneschi V, Cusini M (2016). “Syphilis as “the great imitator”: a case of impetiginoid syphiloderm”. Int J Dermatol. 55 (3): e162–3. doi:10.1111/ijd.13072. PMID 26566601.
  9. ↑ Kimura U, Yokoyama K, Hiruma M, Kano R, Takamori K, Suga Y (2015). “Tinea faciei caused by Trichophyton mentagrophytes (molecular type Arthroderma benhamiae ) mimics impetigo : a case report and literature review of cases in Japan”. Med Mycol J. 56 (1): E1–5. doi:10.3314/mmj.56.E1. PMID 25855021.
  10. ↑ CEDEF (2012). “[Item 87–Mucocutaneous bacterial infections]”. Ann Dermatol Venereol. 139 (11 Suppl): A32–9. doi:10.1016/j.annder.2012.01.002. PMID 23176858.
Diagnosis

Diagnosis

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]
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

Treatment

Medical Therapy

  • 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
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
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

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

Primary Prevention

  • 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)
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)

‘
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)

‘
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

  • 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
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

References

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