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Is Meningitis Transmissible? What are its Potential Complications?

Dr. Khalid is a physician, a researcher, a health writer, and holds a Ph.D. in clinical research.

Is Meningitis Treatable?

Is Meningitis Treatable?

What is Meningitis?

The inflammation of meninges (of the brain and spinal cord) leads to the development of meningitis. The structure of meninges includes pia mater, arachnoid mater, and dura mater (Hersi, Gonzalez, & Kondamudi, 2020). The meninges line the structures of the spinal cord, brain, and vertebral canal. The term ‘Meningitis’ was coined by John Abercrombie in the year of 2015. Meningitis caused 379,000 deaths worldwide despite the availability of vaccination, treatment, and diagnostic procedures. Meningitis reportedly infected 8.7 million individuals in 2015. The virus or bacterial invasion is the preliminary cause of meningitis and its comorbidities. Meningitis is a serious, debilitating, and life-threatening illness that causes severe disabilities in a variety of clinical scenarios. This condition reportedly causes 25% mortalities on a global scale. Meningitis progresses through a marked elevation in CSF (cerebrospinal fluid) cells (Logan & MacMahon, 2008).

What are the Different Types of Meningitis?

Meningitis is categorized into the following types (CDC, 2020) (Hoffman & Weber, 2009) (Logan & MacMahon, 2008).

1. Bacterial meningitis is the most commonly reported meningitis that progresses through bacterial invasion and warrants prompt medical intervention. The highly aggressive meningitis pathogens include Neisseria meningitidis and Streptococcus pneumoniae. It is a life-threatening condition that could lead to potential clinical complications. Some types of bacterial meningitis could be prevented with the help of vaccines. The clinical differentiation of viral and bacterial meningitis appears infeasible. Eventually, the suspected cases require hospitalizations for diagnostic assessment.

2. Viral meningitis is a less severe form of infection as compared to bacterial meningitis. It progresses through viral invasion and potentially impacts the human immune system. However, individuals with a strong immune system have a greater scope of recovery from viral meningitis. Some of the vaccines claim to prevent a few types of viral meningitis. Lumbar puncture is the only intervention warranted to differentiate between viral and bacterial meningitis. Viral meningitis predominantly impacts young children. However, the disease incidence reduces with age advancement of individuals. Viral meningitis in most of the clinical scenarios develops under the impact of enteroviruses. Despite the self-limiting nature of viral meningitis, the disease has the potential to cause considerable morbidity. Herpes simplex in many cases also leads to the development of viral meningitis. Genital herpes is also a risk factor of viral meningitis. HIV seroconversion increases the risk of meningitis to many folds. The patients infected with viral meningitis without associated encephalitis experience an improvement in their prognostic outcomes.

3. Fungal meningitis is a rare condition that progresses following the inhalation of fungal spores through environmental exposure. The patients affected with HIV, cancer, and diabetes experience a greater predisposition towards fungal meningitis.

4. Parasitic meningitis is a rare condition that develops through the invasion of parasites (other than virus and bacteria).

5. Amebic meningitis or PAM (Primary Amebic Meningoencephalitis) occurs under the impact of Naegleria fowleri following the exposure of high-risk individuals to soil and warm water.

6. Non-infectious meningitis develops as a potential complication of head injury, drug(s) exposure, systemic lupus erythematosus, and cancers.

7. Aseptic meningitis manifests through CSF’s pleocytosis, fever, and meningeal symptoms. However, such type of meningitis is not detected through routine bacterial culture.

8. Mononuclear pleocytosis predominantly develops under the sustained impact of mononuclear cells and WBC (white blood cell count) elevation in the CSF.

9. Meningoencephalitis progresses through the clinical manifestations of parenchymal and meningeal diseases and central nervous system (CNS) infection.

10. Encephalitis establishes through the progressive development of diffuse/focal neurological signs and altered mental status under the impact of cerebral cortex disease and brain parenchyma inflammation.

What are the Potential Causes of Meningitis?

The below-mentioned factors, circumstances, pathogens, medical procedures, and disease conditions potentially elevate the risk of meningitis and its clinical complications (Hersi, Gonzalez, & Kondamudi, 2020).

  1. Splenectomy
  2. Sickle cell anemia
  3. Intravenous medication administration
  4. Dural defects
  5. Malignancy/cancers
  6. Bacterial endocarditis
  7. VP (ventriculoperitoneal shunt)
  8. Alcohol use disorder
  9. Exposure to vectors including ticks and mosquitoes
  10. Travel across endemic locations
  11. Exposure to or residence in crowded locations
  12. Immunocompromised states including AIDS and congenital immunodeficiencies
  13. Autoimmune disorders
  14. Organ transplant status
  15. Iatrogenic conditions based on medical interventions
  16. Non-adherence to the vaccination schedule
  17. Age extremes
  18. Chronic diseases including cystic fibrosis, adrenal insufficiency, diabetes, and liver failure
  19. Drug reactions
  20. Paraneoplastic syndromes
  21. Exposure to Listeria monocytogenes
  22. Exposure to Haemophilus influenzae
  23. Exposure to Neisseria meningitidis
  24. Exposure to group B Streptococcus
  25. Exposure to Streptococcus pneumoniae
  26. Exposure to Coccidioides immitis/Coccidiomycosis
  27. Exposure to Cryptococcus neoformans
  28. Exposure to close contacts including college dorms and military barracks
  29. Mucormycosis
  30. Candidiasis
  31. Aspergillosis

What are the Clinical Signs and Symptoms of Meningitis?

The clinical presentation of meningitis is based on the following manifestations and/or their varied combinations (Runde & Hafner, 2020).

  1. Fever
  2. Neck stiffness or pain
  3. Photophobia
  4. Headache
  5. Dizziness
  6. Confusion
  7. Delirium
  8. Irritability
  9. Nausea
  10. Vomiting
  11. Intracranial pressure elevation
  12. Seizures
  13. Neurological deficits
  14. Altered mental status
  15. Obtundation
  16. Focal neurological deficits
  17. Nuchal rigidity
  18. Positive Brudzinski's sign (i.e. involuntary knee flexion following passive neck flexion)
  19. Positive Kernig’s sign (i.e. hip flexion induced pain in supine position following an extension of the knee)
  20. Papilledema (fundoscopic finding)
  21. Purpura fulminans/petechial rash, indicating meningococcal infection
Clinical Manifestations of Meningitis

Clinical Manifestations of Meningitis

What are the Potential Complications of Bacterial Meningitis?

Bacterial meningitis manifests through the development of high-grade bacteremia that potentially invades CNS and bloodstream (Hoffman & Weber, 2009). The bacteria invade the central nervous system by causing local infection or dural defects, identified through MRI/CCT scans. The research studies have yet to determine the actual anatomical location of bloodstream infection. Some of the experimental studies, however, claim choroid plexus as the location of bacterial invasion. Meningococci infect meninges and choroid plexus; however, the leptomeningeal blood vessels are invaded by pneumococci infiltrate. The evidence-based research literature reveals the highly vascularized anatomical locations as the potential entry points for bacterial invasion (Hoffman & Weber, 2009). The molecular tools of the meningeal pathogens help them to invade CSF barriers based on stringent junctions and complex structures. The Streptococci protein structures encompass the blood-brain barrier following their interaction with phosphorylcholine’s glycoconjugate receptors and eukaryotic cells’ PAF (platelet-activating factor). This eventually triggers endocytosis that leads to the passage of bacterial proteins (including CbpA) through the blood-brain barrier. The integrins and vitronectin interact with the outer membrane protein; however, CD-46 interacts PilC1 adhesin of meningococci (Hoffman & Weber, 2009). The adhesive proteins of Escherichia coli and GBS (group B streptococcal) facilitate their entry into the central nervous system of the newborn babies.

The bacterial invasion progresses through the endothelial cells’ inflammatory activation and ICAM-1 (i.e. adhesion molecular) regulation (Hoffman & Weber, 2009). This episode actively triggers leucocyte invasion that leads to the accumulation of NO (nitric oxide) and MMPs (matrix metalloproteinases) across the CSF/blood-brain barrier. The bacterial invasion, replication, and autolysis across the subarachnoid space unprecedentedly intensify the inflammatory processes. The bacterial invasion also triggers the production of mast cells, perivascular macrophages, and endothelial cells. Interestingly, other than living bacteria, PAMP (pathogen-associated molecular patterns) and the heat-killed bacteria also trigger meningitis in a variety of clinical scenarios. This type of meningitis predominantly occurs under the impact of pathogens including LPS (lipopolysaccharides), PG (peptidoglycan), LTA (lipoteichoic acid), and LP (lipoprotein) (Hoffman & Weber, 2009). The tracking and identification of PAMPs occur through sensors based on immune pattern recognition molecules including LBP and CD14. Similarly, TLR2 recognition occurs through pneumococcal LP and PG. TLR4 plays a predominant role in the signaling of pneumococcal toxin pneumolysin and LPS. MyD88 is an intracellular adaptor protein that channelizes the TLR signals to MAP/NFkB kinases (i.e. inflammatory signaling cascades) that eventually trigger rapid inflammatory responses in the infected patients.

The highly debilitating neurological deficits potentially deteriorate the survival and health-related quality of life of the bacterial meningitis survivors (Hoffman & Weber, 2009). The hippocampus atrophy in meningitis patients is preceded by neuronal loss, identified through magnetic resonance imaging. The diffusion of CSF with extracellular fluid elevates the activity of inflammatory toxic mediators and soluble bacteria in meningitis infected patients. The neuronal damage is accompanied by intracranial complications, immune-competent cells’ cytotoxic products, and bacterial toxins (Hoffman & Weber, 2009). Some of the major toxins include pneumolysin and hydrogen peroxide, particularly in the scenario of Streptococcus pneumoniae. These toxins, in many scenarios, cause irreversible damage to mitochondria that eventually triggers the death processes of microglia and neurons.

Is Meningitis a Transmissible or Communicable Disease?

  1. Most forms of bacterial and viral meningitis are communicable or transmitted from one person to another.
  2. Bacterial meningitis communicates through the throat or respiratory secretions.
  3. The risk factors for bacterial meningitis transmission include unhygienic conditions, use of unwashed utensils, kissing, sneezing, and coughing (Indiana University, 2019).
  4. The consumption of contaminated food and contact with feces also greatly increases the risk of meningitis transmission (Davis, 2018).

What are the Diagnostic Measures for Meningitis Assessment?

The following diagnostic interventions are highly warranted to evaluate or rule out the occurrence of bacterial meningitis (Tacon & Flower, 2012).

  1. Complete blood count assists in evaluating neutrophilia, a predominant marker of infection
  2. Serum glucose facilitates CSF glucose interpretation
  3. Creatinine, BUN, and electrolyte levels assist in determining fluid management strategies
  4. Coagulation profile helps to evaluate potential vascular complications of meningitis
  5. Blood culture assessments help in tracking 40% to 90% of bacterial meningitis cases
  6. Inflammatory markers, including procalcitonin and CRP
  7. CSF lactate
  8. CSF PCR
  9. CSF latex agglutination
  10. Culture and sensitivity (microscopic) study based on gram staining helps to identify the causative organisms including gram-positive cocci (i.e. S. pneumoniae), gram-negative cocci (i.e. N. menigitidis), and gram-negative rod (i.e. H. influenzae)
  11. CSF-glucose and protein
  12. CT head assists in evaluating/ruling out meningitis-related conditions including, neurological dysfunction, ICP elevation, focal neurologic complications, infarction, subdural empyema, abscess, and hydrocephalus
  13. PCR on urine or blood

What are the Treatment Interventions/Approaches for the Clinical Management of Meningitis?

The conservative treatment of meningitis warrants the administration of the below-mentioned pharmacotherapeutic agents based on the age of the patients and/or type of meningitis (Hersi, Gonzalez, & Kondamudi, 2020). s

  1. Treatment of cryptococcal or fungal meningitis is based on the administration of flucytosine (oral) and amphotericin B (intravenous)
  2. The meningitis patients allergic to penicillin could be treated with intravenous vancomycin or moxifloxacin
  3. The patients who develop meningitis due to penetrating trauma or post-procedure foreign body require intravenous vancomycin or meropenem or ceftazidime or cefepime
  4. The immunocompromised middle-aged adults (of greater than 50 years of age) could receive intravenous ampicillin, or vancomycin, or ceftriaxone for their meningitis management
  5. The intravenous ceftriaxone and vancomycin appear to be the best treatment option for the clinical management of meningitis in patients between the age group of 18-49 years
  6. The intravenous ceftriaxone or ampicillin effectively control meningitis manifestations in children above 1 month of age
  7. Meningitis infected neonates (i.e. below 12 months of age) could be treated through intravenous acyclovir, or gentamycin, or cefepime, or ceftazidime, or cefotaxime or ampicillin
  8. Ceftriaxone is a 3rd generation cephalosporin that effectively treats gram-negative organisms including Neisseria meningitidis and Streptococcus pneumoniae
  9. Ceftriaxone has a greater capacity to penetrate CNS as compared to piperacillin-tazobactam
  10. Ceftriaxone is a treatment of choice for the clinical management of gram-negative sepsis
  11. Vancomycin effectively treats meningitis related to the invasion of methicillin-resistant Staphylococcus aureus
  12. Vancomycin is a treatment of choice for the clinical management of meningitis that emanates following the invasion of gram-positive bacteria and resistant pneumococcus
  13. Ampicillin effectively treats Listeria and other gram-positive bacilli
  14. Cefepime is a 4th generation cephalosporin having the potential to treat meningitis emanating from pseudomonas invasion
  15. Cefotaxime is a 3rd generation cephalosporin with a safety profile for neonates
  16. The clinical management of cerebral perfusion is essentially required for the meningitis patients affected with elevated intracranial pressure (ICP) and related manifestations including bradycardia, non-reactive pupils, neurologic deficits, and altered mental status
  17. ICP management in meningitis warrants 30 degrees elevation of the patient bed’s head
  18. ICP management also requires intubation and mild hyperventilation induction
  19. The pharmacotherapeutic management of ICP warrants the administration of osmotic diuretics including 3% saline and 25% mannitol
  20. Chemoprophylaxis is highly recommended for the close contacts of a meningitis patient infected with H. influenzae type B and/or Neisseria meningitidis
  21. The close contacts of meningitis patient (infected with N. meningitidis) require clinical management based on ceftriaxone, or ciprofloxacin, and/or rifampicin
  22. Rifampicin is the treatment of choice for clinically managing a close contact of the meningitis patient infected with N. meningitidis

References

CDC. (2020, 01 21). Meningitis . Retrieved from https://www.cdc.gov/meningitis/index.html

Davis , C. P. (2018). Is Meningitis Contagious? Medicine Net.

Hersi, K., Gonzalez, F. J., & Kondamudi, N. P. (2020). Meningitis. In StatPearls. Treasure Island (Florida): StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK459360/

Hoffman, O., & Weber , R. J. (2009). Pathophysiology and Treatment of Bacterial Meningitis. Therapeutic Advances in Neurological Disorders, 2(6), 1-7. doi:10.1177/1756285609337975

Indiana University. (2019). Bacterial and viral meningitis. Retrieved from Protect IU : https://protect.iu.edu/environmental-health/public-health/communicable-diseases/meningitis.html

Logan, S. A., & MacMahon, E. (2008). Viral meningitis. BMJ, 336(7634), 36-40. doi:10.1136/bmj.39409.673657.AE

Runde, T. J., & Hafner, J. W. (2020). Meningitis, Bacterial. In StatPearls. Treasure Island (Florida): StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK470351/#_article-24965_s4_

Tacon, C. L., & Flower , O. (2012). Diagnosis and management of bacterial meningitis in the paediatric population: A review. Emergency Medicine International. doi:10.1155/2012/320309

This content is for informational purposes only and does not substitute for formal and individualized diagnosis, prognosis, treatment, prescription, and/or dietary advice from a licensed medical professional. Do not stop or alter your current course of treatment. If pregnant or nursing, consult with a qualified provider on an individual basis. Seek immediate help if you are experiencing a medical emergency.

© 2020 Dr Khalid Rahman

Discussion

Sarahkhalid on April 23, 2020:

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