CNS syndromes,pyogenic meningitis Flashcards
Leptomeninges
Arachnoid and pia mater
Modes of spread of CNS infections
- Hematogenous spread
- Direct spread
- Anatomical defect
- Direct intraneural spread
Infective syndromes of CNS
1. Meningitis: • acute bacterial • acute viral • chronic 2. Encephalitis and encephalopathy: 3. Space occupying lesions: • focal CNS lesions • cystic parasitic diseases 4. Other
Types of meningitis
Acute meningitis:
progresses rapidly in a few hours. It can be further grouped acute bacterial (or pyogenic) and acute viral meningitis
Chronic meningitis: Progressively worsens over weeks (>4 weeks). This includes bacterial, parasitic, fungal agents and viral agents.
Some of the agents of chronic meningitis have a subacute course that progressively worsens over several days.
Host reaction to meningitis
The host inflammatory response in meningitis may vary—acute bacterial meningitis - 🔼 neutrophil count in CSF, whereas
both acute viral meningitis and chronic meningitis are predominantly lymphocytic
Chronic meningitis types
- Chronic persistent meningitis:
In most of the cases, the symptoms are chronic and persistent
2. Chronic recurrent meningitis: Characterized by discrete episodes of illness along with the absence of symptoms with normal CSF parameters between episodes.
Eg., Mollaret’s meningitis, caused by HSV type 2
Aseptic meningitis
Traditionally used to describe those meningitis, where the infectious etiology is unidentified. This used to include agents other than bacteria such as the agents of acute viral meningitis and chronic meningitis. However in the modern era of sophisticated diagnostic facility (e.g. molecular methods), it is now possible to detect most of these agents
Clinical manifestations of meningitis
Patients with meningitis present with high-grade fever, 🤮, headache, neck rigidity and certain unique signs: Kernig’s and Brudzinski’s signs
Manifestations of encephalitis
The common manifestations include altered consciousness, behavioral changes, seizures, focal neurological deficits and sometimes, extrapyramidal signs such as involuntary movements
The cellular infiltrate present in the CSF is typically lymphocytic rather than neutrophilic
Agents of encephalitis
1. Viruses: • rabies • herpes • arboviruses such as JE & West Nile viruses 2. Parasites: • Toxoplasma gondii • Naegleria fowleri
meningoencephalitis
Very often, encephalitis is associated with concomitant meningitis; called as meningoencephalitis (e.g. primary amoebic meningoencephalitis, caused by a free-living amoeba called Naegleria fowleri)
Brain abscesses
source of infection
- Contiguous infection of the adjacent structures such as sinuses, middle ear or mastoids (45%–50%)
2. Hematogenous:
especially in patients with cyanotic congenital heart disease (25%) - Direct inoculation as a result of trauma or surgery (10%)
4. Cryptogenic: In at least 15% of cases, the source of the infection is unknown.
Brain abscesses in immunocompetent individuals
1. Streptococci: M/C anaerobic, aerobic, and viridans group (e.g. S. anginosis) 2. Anaerobes: Bacteroides fragilis, Fusobacterium 3. Enterobacteriaceae: Proteus, E. coli, Klebsiella 4. Staphylococcus aureus: Usually in post-trauma or post-neurosurgery cases
Brain abscesses in immunocompromised hosts
- Nocardia
- Toxoplasma gondii
- Aspergillus
- Candida and Cryptococcus
- Taenia solium (neurocysticercosis):
especially in Latin America
6. M. tuberculosis (tuberculoma):
especially in India and East Asia
Brain abscesses
clinical features
Triad of: 1. 🤒 2. Severe headache (unilateral, on the side of the abscess) 3. Focal neurologic deficit constitute the major manifestations
Brain abscess
treatment
1. Surgical excision or drainage of the abscess combined with prolonged antibiotics (for 6-8 weeks) remains the treatment of choice
2. Ceftriaxone plus metronidazole is the preferred regimen, if bacterial etiology is suspected
Subdural Empyema
- Subdural empyema (or abscess) is an intracranial focal collection of purulent material located between the dura mater and the arachnoid
- 95% confined to frontal lobe.
- Source of infection, etiological agents and clinical presentation are similar to that described for brain abscess.
Suppurative Intracranial Thrombophlebitis
Septic venous thrombosis of cortical veins and sinuses such as cavernous sinus, the lateral sinus, or the superior sagittal sinus.
• Cavernous sinus thrombophlebitis occurs secondary to infection of sinuses (sphenoid and ethmoid sinuses) and oral cavity
• Septic phlebitis of the lateral sinuses is associated with mastoiditis and otitis media
Infectious myelitis
Inflammation of the spinal cord which can result in disruption of the connection from the brain to the rest of the body, and vice-versa. It may have either infectious or autoimmune etiology.
- Viral myelitis: M/C
e. g. poliovirus - Non-viral: rare
Acute encephalitis syndrome (AES)
clinical presentation
AES presents with acute-onset of fever and a change in mental status (mental confusion, disorientation, delirium, or coma) and/or new-onset of seizures
• Japanese encephalitis virus (JEV) M/C in India (ranging from 5%-35%)
• The etiology in a large number of AES cases still remains unidentified.
Agents of pyogenic meningitis
(overall)
- Streptococcus pneumoniae: M/C (~50%)
- Meningococcus (~25%)
- Streptococcus agalactiae(~15%)
- Listeria (~10%)
- Haemophilus influenzae (<10%)
Acute bacterial meningitis in neonates
- Streptococcus agalactiae (elderly also)
- Gram-negative bacilli such as E coli and Klebsiella
- Listeria monocytogenes (elderly also)
Transmission of acute bacterial meningitis
Bacteria that cause acute meningitis are transmitted through:
- Droplets M/C
- Close and prolonged contact—kissing, sneezing or coughing on someone, or living in close quarters with an infected person facilitate the spread of the disease.
Acute bacterial meningitis
routes of spread
- Hematogenous spread:M/C
through the choroid plexus or through other blood vessels
2. Direct spread from an infected site present close to meninges—otitis media, mastoiditis, sinusitis, etc.
3. Anatomical defect in central nervous system (CNS):
surgery, trauma, congenital defects,
Neonates have the highest prevalence of meningitis; probably due to
- Immature immune system,
- Microbes of mother’s
birth canal (e.g. Listeria or Streptococcus agalactiae) - 🔼 permeability of blood brain barrier
Predisposing factors of pyogenic meningitis
- Age: neonates are more susceptible
- Vaccination status
- Factors that promote infection at 1° site: respiratory
- Presence of CSF shunts
- Breach in BBB
Symptoms of pyogenic meningitis
- 🤒
- 🤮
- Intense headache
- Altered consciousness
- Occasionally photophobia
Signs of pyogenic meningitis
1. Nuchal rigidity (“stiff neck”) specific:
neck resists passive flexion
2. Kernig’s sign:
Severe stiffness of the hamstrings ➡️ inability to straighten the leg when the hip is flexed to 90°
3. Brudzinski’s sign: When the neck is passively flexed, results in spontaneous flexion of the hips and knees
Manifestations of pyogenic meningitis in infants
Pyogenic meningitis in infants may have a slower onset, signs may be nonspecific, and neck stiffness may not be present. Babies usually present with fever, irritability and bulging fontanelle
Specimen collection of pyogenic meningitis
CSF is obtained by lumbar puncture under strict aseptic conditions.
It is divided into three sterile containers;
1. cell count
2. biochemical analysis
3. bacteriological examination
Specimen transport of pyogenic meningitis
CSF should be examined immediately
• When the bacteriological examination (culture) is required, it should never be refrigerated as delicate pathogens such as H. influenzae, pneumococci or meningococci may die
➡️ if a delay is expected, it may be kept in an incubator at 37°C
• However for molecular diagnosis, CSF can be kept inside the freezer
Specimen collection & transport for suspected meningococcal meningitis
Lumbar puncture. Other useful specimens are nasopharyngeal swabs, pus or scrapings from rashes; carried in transport media (such as Stuart’s medium).
• These specimens are inoculated onto selective media, such as Thayer Martin medium or New York City medium, to suppress the growth of normal flora
Cytological and biochemical parameters in CSF of pyogenic meningitis
- CSF pressure: >180
- TLC: 100-10,000
- Neutrophils predominant
- Glucose <40 mg
Decreased to absent - Total proteins:
>45 mg/dL
Heaped smear
As the bacterial load in CSF may be very low, to increase the sensitivity, several drops of CSF should be placed at the same spot on the slide, each drop being allowed to air dry before the next is added
Centrifugation can be used
Direct antigen test for pyogenic meningitis
- From CSF:
Latex agglutination test for detection of capsular antigens of agents of meningitis such as S. pneumoniae, S. agalactiae, N. meningitidis, H. influenzae or E. coli
(Antigen detection is more sensitive than CSF microscopy) - From urine:
Immunochromatographic test (ICT) is available to detect the C-polysaccharide antigen of S. pneumoniae in urine.
Culture of agents of pyogenic meningitis
- Enriching:
Bacterial load 🔽➡️ a part of the CSF is inoculated into enriched media such as blood culture bottles at the bed side (preferred) or BHI broth in the laboratory
2. Blood culture can be collected in conventional blood culture bottles such as BHI broth/agar or preferably in automated blood cultures
