Meningitis: Purulent and Aseptic

June 17, 2021 Gaurab Karki Microbiology 0




Meningitis: Purulent and Aseptic
Meningitis: Purulent and Aseptic

What is Meningitis?

  • The infection within the subarachnoid space or throughout the leptomeninges is called meningitis.
  • Meningitis is divided into two major categories based on the host’s response to the invading microorganism. They are:
    • purulent meningitis
    • aseptic meningitis.

 1. Purulent meningitis

  • A patient with purulent meningitis typically has a marked, acute inflammatory exudative cerebral spinal fluid containing large numbers of polymorphonuclear cells (PMNs).
  • The underlying CNS tissue, in particular the ventricles, may be involved.
  • Ventriculitis means the involvement of ventricles.
  • The cause of these infections is bacterial organisms.

Pathogenesis of purulent meningitis:

  • Within the Central Nervous System, the blood-brain barrier is the important host defense mechanism.
  • This barrier involves the choroid plexus, arachnoid membrane, and the cerebral microvascular endothelium.
  • Vascular endothelium has got the unique structural properties.
  • There is the presence of continuous intercellular tight junctions.
  • It minimizes the passage of infectious agents into the CSF and acts as a barrier.
  • The vascular endothelium helps in regulating the transport of nutrients in and out of the CSF.
  • It includes low-molecular-weight plasma proteins, glucose, and electrolytes.
  • Different underlying conditions and the host’s age may be responsible for the development of infectious meningitis.
  • The highest rate of infection of meningitis is in neonates.
  • It is because of the:
    • the immature neonatal immune system
    • the increased permeability of the blood-brain barrier in newborns
  • The presence of colonizing bacteria in the female vaginal tract
  • The most common bacterial pathogens responsible for meningitis in newborns are:
    • Group B streptococci
    • Escherichia coli
    • Listeria monocytogenes
  • Before the development of the vaccine i.e Hib vaccine, the common cause of meningitis is Haemophilus influenza type b.
  • It occurred in children of 4 months to 5 years of age.
  • There is a decline in the Hib disease because of this childhood immunization program.
  • Neisseria meningitidis causes meningitis in young adults.

Two meningococcal vaccines (vaccines for N. meningitidis) are available:

  • The meningococcal polysaccharide vaccine (MPSV4): for older than 55 years of age
  • The meningococcal conjugate vaccine (MCV4): for adolescents.
  • The cause of meningitis in young children and elderly people is Streptococcus pneumonia.
  • This meningitis develops from bacteremia or infection of the sinuses or middle ear.

Two pneumococcal vaccines (vaccines for S. pneumoniae) are:

  • The pneumococcal conjugate vaccine (PCV13):
  • protects against infection from 13 different serotypes of pneumonia
  • used for vaccination of children and adults.
  • Pneumococcal polysaccharide vaccine (PPSV):
    • protects from 23 serotypes of pneumonia
    • recommended vaccine for adults 65 years of age and older
    • recommended vaccine for anyone over the age of 2 who has long-term health problems or is immunocompromised.
  • The primary portal of entry for causative agents of meningitis is the respiratory tract.
  • Predisposing factors of meningitis to the adults are usually the same factors that cause pneumonia or other respiratory tract colonization or infection.
  • Increased risk in:
    • Alcoholism
    • Splenectomy
    • diabetes mellitus
    • prosthetic devices
    • immunosuppression
  • Patients with prosthetic devices, particularly CNS and ventriculoperitoneal shunts, are at increased risk for developing meningitis.
  • Host defense mechanisms must be overcome by the organism to reach the CNS (primarily by the blood-borne route).
  • The pathogen should colonize and cross the host mucosal epithelium.
  • Then it should enter and thrive within the bloodstream.
  • Pathogen should be able to evade the host defenses at each level.
  • By breaking the blood-brain barrier at the level of microvascular endothelium, helps the organism to enter the CNS.

Virulence factors of Streptococcus pneumoniae:

  • IgA protease: It is secreted by the Streptococcus pneumoniae and meningitidis. It can destroy the host’s secretory IgA and helps in bacterial attachment to the epithelium.
  • Capsule: It is antiphagocytic and helps to evade destruction by the host immune system.
  • Pili
  • polysaccharide capsules
  • lipoteichoic acids
  • Organisms can enter by
    • disrupting tight junctions of the blood-brain barrier
    • transport within circulating phagocytic cells
    • crossing the endothelial cell lining within endothelial cell vacuoles.
  • Then multiplication occurs within the CSF.

Clinical Manifestation of purulent meningitis:

i). Acute meningitis

  • Symptoms of acute meningitis include:
    • Fever
    • stiff neck
    • headache
    • nausea and vomiting
    • neurologic abnormalities
    • change in mental status.
    • Presence of large numbers of inflammatory cells (>1000/mm3), primarily polymorphonuclear cells (PMNs) in the CSF.
  • In CSF there is:
    • decreased glucose level relative to the serum glucose level
    • an increase in protein concentration.
    • In Normal condition:
      • The normal CSF glucose level is 0.6 of the serum glucose level and ranges from 45 to 100 mg/dL
      • The CSF protein range in an adult is 15 to 50 mg/dL; newborn CSF protein ranges run as high as 170 mg/dL with an average of 90 mg/dL.
  • The sequelae of acute bacterial meningitis in children are frequent and serious. It includes:
    • Seizures
    • cerebral edema
    • hydrocephalus
    • cerebral herniation
    • focal neurologic changes.
  • In about 10% of children recovering from bacterial meningitis, permanent deafness can occur.

ii). Chronic Meningitis

  • May occur in immunocompromised patients.
  • Symptoms:
    • Fever
    • Headache
    • stiff neck
    • nausea and vomiting,
    • Lethargy
    • Confusion
    • mental deterioration.
  • Symptoms may persist for a month or longer before treatment is sought.
  • Manifestation in CSF:
    • an abnormal number of white blood cells (usually lymphocytic)
    • elevated protein
    • decrease in glucose content

The pathogenesis of chronic meningitis is similar to that of acute disease.

Etiologic agents of Chronic Meningitis:

  • HIV cytomegalovirus
  • Enterovirus
  • HSV
  • Mycobacterium tuberculosis
  • Cryptococcus neoformans
  • Coccidioides immitis
  • Histoplasma capsulatum
  • Blastomyces dermatitidis
  • Candida
  • Aspergillosis
  • Mucormycosis
  • Miscellaneous other fungi
  • Nocardia
  • Actinomyces
  • Treponema pallidum
  • Brucella
  • Borrelia burgdorferi
  • Sporothrix schenckii
  • Rare parasites—Toxoplasma gondii, cysticercus, Paragonimus westermani, Trichinella spiralis, Schistosoma , Acanthamoeba

2. Aseptic meningitis:

  • It is usually viral and characterized by an increase of lymphocytes and other mononuclear cells (pleocytosis) in the CSF
  • Bacterial and fungal cultures are negative.
  • It is usually self-limiting.
  • Symptoms:
    • Fever
    • Headache
    • Stiff neck
    • nausea, and vomiting
  • Increase of lymphocytes and other mononuclear cells in the CSF
  • Normal glucose level
  • Normal or slightly elevated protein CSF level.
  • Aseptic meningitis can also be a symptom for syphilis and some other spirochete diseases (e.g., leptospirosis and Lyme borreliosis).
  • Stiff neck and CSF pleocytosis may also be associated with other disease processes, such as malignancy.