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Introductory Microbiology > Central Nervous System Infections > Flashcards

Central Nervous System Infections Flashcards

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1
Q

What are the most common CNS infections?

A
  • Meningitis: inflammation of the meninges
  • Encephalitis: inflammation of the brain
  • Brain abscess: area of pus within the brain; not an infection OF the brain
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2
Q

What classes of pathogens may cause CNS infections?

A
  • mainly bacterial and viral; viral are more common but bacterial more serious
  • also can be caused by certain fungi and parasites
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3
Q

How does the blood-brain barrier (BBB) act as a defence mechanism for the CNS?

A
  • capillaries limit access of immune cells and pathogen to CSF and brain tissue; very tight junctions that only lipid soluble and very small substances can travel through
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4
Q

What challenge may the BBB propose?

A
  • pharmacotherapy

- limits the number of antibiotics that are able to cross the BBB

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5
Q

How does inflammation have positive implications for CNS infections?

A
  • loosening of tight junctions and increased capillary permeability allow immune cells and medications to pass the BBB
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6
Q

What innate host factors put one at risk for CNS infections?

A

1) absence of normal flora
2) paucity of local macrophages, antibodies and complement
3) inflammation; increases permeability of the BBB facilitating pathogen entry

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7
Q

What portals of infection allow pathogens to access the CNS?

A
  • trauma to bones and meninges or medical procedures
  • peripheral neurons (ex. rabies)
  • respiratory system; bacteremia
  • gastrointestinal system; bacteremia (frail elderly, pregnant women and young are vulnerable to infection via GI)
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8
Q

What is acute meningitis?

A
  • caused by infection, usually bacterial
  • symptom duration < 2 weeks, patients are seriously ill
  • considered a medical emergency
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9
Q

What is chronic and aseptic meningitis?

A
  • due to viral illness, immunocompromised patients, or associated with a reaction to drugs
  • symptom duration of more than 2 weeks, variable severity of symptoms
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10
Q

What are the clinical findings of meningitis?

A

Systemic infection: fever, myalgia, rash

Meningeal inflammation: neck stiffness, Brudzinski’s sign, Kernig’s sign, jolt accentuation of headache

Cerebral vasculitis: seizures

Elevated Intracranial pressure: headache, N/V, change in mental status, neurologic symptoms, seizures

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11
Q

What is rash in meningitis associated with?

A

Gram negative bacteria (Neisseria meningitidis or Listeria monocytogenes; release endotoxins)

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12
Q

What information is needed when making a diagnosis of meningitis?

A
  • patient history; previous RT infection, past antibiotic use, medications, food intake, etc.
  • symptoms and signs
  • physical exam
  • lab tests; blood, CSF analysis and culture
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13
Q

What are the symptoms and signs of meningitis?

A

Symptoms: chills, neck stiffness, headache, altered mental state, focal neurological deficits, seizure, photophobia, nausea & vomiting

Signs: fever, nuchal rigidity, Brudzinski & Kernig signs, jolt accentuation of headache, Glasgow coma scale (GCS), rash

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14
Q

What is the classic clinical triad of meningitis?

A
  • fever, nuchal rigidity, headache
  • present in 44% of cases
  • absence of all three rules out meningitis
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15
Q

95% of clients with meningitis exhibit 2 of these 4 signs/symptoms:

A

1) headache
2) fever
3) nuchal rigidity
4) altered mental state

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16
Q

What is nuchal rigidity?

A
  • inability to flex neck forward due to rigidity of the neck muscles; if flexion of the neck is painful, but full range of motion is present, nuchal rigidity is considered absent
  • client will resist movement when pressure is applied
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17
Q

What is Brudzinski’s sign?

A
  • passive neck flexion in supine position leads to flexion of knees and hips
  • a way of relieving the tension and pressure from increased ICP
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18
Q

What is Kerning’s sign?

A
  • extension of knee with patient supine and hip flexed at 90 degrees results in resistance or pain in lower back or posterior thigh
  • client is resistant to straightening of leg
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19
Q

What is jolt accentuation of headache?

A
  • accentuation (worsening) of headache with active horizontal head turning at a frequency of 2-3 turns per second
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20
Q

Absence of jolt accentuation, Brudzinski or Kerning signs cannot…

A

RULE OUT meningitis if clients with fever headache and altered mental state

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21
Q

What test is recommended for those with a suspected case of meningitis?

A
  • lumbar puncture for CSF analysis
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22
Q

What will a CSF analysis reveal in bacterial meningitis?

A
  • low CSF glucose levels (< 2.5 mmol/L or < 40% of serum glucose - 60% is normal)
  • high CSF protein levels (> 0.45 g/L)
  • CSF pleocytosis (500 - 20,000 WBC/mm^3); >80% neutrophils
  • lumbar puncture opening pressure will be higher
  • Gram stain and culture
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23
Q

What will a CSF analysis reveal in viral meningitis?

A
  • normal CSF glucose levels
  • normal to mildly increased CSF protein levels
  • CSF WBC elevated (10-1000 WBC/mm^3); mainly lymphocytes and monocytes
24
Q

Why is CSF glucose lower in cases of bacterial meningitis?

A
  • inflammation of the meninges leads to decreased glucose receptor expression
  • glucose transport from the blood into the CSF is impaired
  • this level of inflammation is not seen with viral meningitis
25
Q

What pathogens cause meningitis?

A

Bacteria:

  • Streptococcus pneumoniae
  • Neisseria meningitidis
  • Haemophilus influenzae
  • Listeria monocytogenes
  • Group B Streptococcus

Viruses:

  • Enteroviruses (Coxsackie B)
  • Herpes Simplex Virus

Fungi & Parasites

26
Q

What is the most common cause of bacterial meningitis?

A
  • Streptococcus pneumoniae, then Neisseria meningitidis
27
Q

What is pneumococcal meningitis and how is it transmitted?

A
  • causative organism of meningitis in all age groups
  • responsible for 50% of cases of bacterial meningitis
  • 75% of us already colonized with S. pneumoniae in nasopharynx
  • in most cases, caused by bacteremia associated with pneumonia
  • transmitted via respiratory droplets
  • infectious period 1-3 days prior to onset of clinical symptoms and 24 hrs post-antibiotic therapy (pathogen no longer present in oral/nasal discharge)
  • fatality rate of 26%
  • 40% of survivors left permanent neurological deficit (ex. hearing loss, blindness, paresis)
28
Q

Is pneumococcal meningitis itself contagious?

A

No; S. pneumoniae can be transmitted but will not cause invasive disease unless you are susceptible

29
Q

What public health implications exist for cases of pneumococcal meningitis?

A
  • all cases reported to public health
  • no droplet precautions necessary; routine precautions only
  • no chemoprophylaxis for close contacts that were exposed
30
Q

Immunizations for pneumococcal meningitis

A
  • targeted at immunizing the client against S. pneumoniae infection
  • routine infant immunization: pneumococcal conjugated vaccine (Pneu-C-13; Prevnar13)
  • pneumococcal polysaccharide vaccine (Pneu-P-23; Pneumovax 23)
31
Q

Who should receive pneumococcal polysaccharide vaccination?

A
  • all Individuals ≥ 65 years of age

- individuals at increased risk for invasive pneumococcal disease (pneumonia, bacteremia, meningitis) ≥ 2 years of age

32
Q

What are microbiological features of Neisseria meningitidis allow it to cause infection?

A
  • some individuals have this organism present in their nasopharynx
  • highly transmittable
  • diplococci shape with capsule and fimbriae for adherence
  • invasins for penetration of respiratory epithelial cells
  • endotoxins cause tissue damage, inflammation and evasion of host defences
  • meningitis results when the bacteria crosses the BBB and multiplies in the subarachnoid space, leading to subarachnoid inflammation, cerebral vasculitis and increased BBB permeability
33
Q

What is meningococcal meningitis and how is it transmitted?

A
  • affects mainly children, adolescents and young adults
  • responsible for 20% of bacterial meningitis cases
  • serogroups A, B, C, Y and W-135 most common in Canada
  • 20% of us colonized with N. meningitidis in nasopharynx; not affected but can transmit to others
  • Gram negative causes endotoxin production
  • transmitted via respiratory droplets
  • infectious period 7 days prior to onset of clinical symptoms and 24 hrs post-antibiotic therapy (pathogen no longer present in oral/nasal discharge)
  • associated with outbreak phenomenon because symptoms do not appear for a week after infection
  • patient must be isolated
  • fatality rate 10%
  • 20% survivors exhibit permanent neurological or physical deficit
34
Q

Why is the younger population more susceptible to meningococcal meningitis?

A
  • younger population spends more time with strangers; daycare, school, college/university
  • high opportunity for transmission
35
Q

What are symptoms of endotoxin production as seen with N. meningitidis?

A
  • chills, fever, weakness, generalized aches, petechial rash
  • presence of organism in blood causes rash to form d/t micro-clots; does not disappear with pressure
  • endotoxic shock and disseminated intravascular coagulation
36
Q

What public health implications exist for cases of meningococcal meningitis?

A
  • all cases reported to public health
  • all suspected or possible cases should be placed in respiratory isolation for 24 hours post-targeted antibiotic therapy
  • “close contacts” must be immunized and receive chemoprophylaxis
  • includes household, child care facility, nursery school contacts
  • individuals in contact with the patient’s oral secretions or who frequently ate/slept in the same dwelling within 7 days of disease onset
37
Q

How is meningococcal meningitis treated?

A
  • rifampin (all ages)

- ciprofloxacin (>18 years of age d/t potential damage to cartilage)

38
Q

Immunizations for meningococcal meningitis

A
  • vaccination recommended to control outbreaks, for patients with increased susceptibility to meningococcal disease, and for travellers
  • Men-C-C; Serogroup C only (2 months – 11 years of age)
  • Men-C-ACYW; Serogroups A, C, Y, W-135 (Grade 7)
  • Bexsero; Serogroup B only (2 months – 17 years of age
39
Q

What is Haemophilus influenzae meningitis and how is it transmitted?

A
  • used to be the leading cause of bacterial meningitis, but dropped by 94% in 1994 due to vaccination
  • commonly seen in communities where children are not vaccinated
  • not the same as influenza virus
  • cases must be reported to public health
  • transmitted via respiratory droplets
  • suspected or possible cases of H. influenzae meningitis; respiratory isolation 24 hrs post targeted antibiotic therapy
  • close contacts should receive chemoprophylaxis (rifampin) & immunization
40
Q

What is listeria monocytogenes and how is it transmitted?

A
  • common in the extremes age, immunodeficiency and pregnant women
  • 10% of all cases of meningitis
  • fatality rate 15%
  • transmitted via ingestion of contaminated foods (soft cheeses, refrigerated unpasteurized foods, deli meats) and poor hand hygiene
  • causes listeriosis, a type of gastroenteritis
  • only routine precautions necessary; wash foods well, avoid unpasteurized foods and deli meats when pregnant or at extremes of age
41
Q

What is group B streptococcal meningitis and how is it transmitted?

A
  • streptococcus agalactiae
  • 30% of women colonized with GBS in reproductive tract; 40 - 70% will transmit during delivery; 1 - 3% of neonates will develop a GBS infection
  • swab in vagina and rectum at 35-37 weeks to determine if the woman is GBS positive
  • if GBS positive, antibiotics are given at the time of labour or membrane rupture
  • given IV, 2 doses 4 hours apart, with the last dose > 2 hours prior to delivery
  • if not treated prior to delivery, neonate blood cultures are done at 24 and 48 hours, or antibiotic prophylaxis to prevent infection
42
Q

What are risk factors for transmission of GBS to the infant during delivery?

A
  • GBS positive, premature labour, elevated temperature, UTI caused by GBS, membrane rupture >18 hrs
43
Q

How is bacterial meningitis treated?

A
  • bacteriocidal antibiotic therapy
  • administered after lumbar puncture, or soon after blood cultures are drawn (if LP is delayed)
  • antibiotic therapy directed at likely pathogens
  • must be able to cross BBB
  • dexamethasone co-administered with antibiotic therapy to decrease inflammation in meninges: decreased risk of death
    and no increase in adverse events
  • supportive measures such as antipyretics, fluids & electrolytes, nutritional support
44
Q

What is viral meningitis and how is it transmitted?

A
  • caused by enteroviruses (Coxsackie B, Echovirus), and Herpes Simplex Virus
  • causes less acute and severe illness compared to bacterial meningitis
  • also called aseptic meningitis
  • treatment is supportive, no cure
  • enteroviruses cause 85% of viral cases
  • transmitted via direct contact and fecal-oral route, most common in summer and fall
  • self-limited illness in those who are immunocompetent
  • lasts 7 to 10 days
  • may not require hospitalization
45
Q

What is encephalitis?

A
  • inflammation of the brain
  • may occur simultaneously with meningitis
  • infectious and non-infectious causes should be considered
  • consider season of the year, geographic locale, prevalence of disease in the local community, travel history, recreational activities, occupational exposure, insect contact, animal contact, vaccination history, and immune status of the patient
  • context can reveal cause
  • viral encephalitis most common with bacterial, fungal and protozoal causes also observed
  • etiology and presentation in immunocompromised patients often different than healthy hosts
46
Q

What are the symptoms and signs of encephalitis?

A
  • changes in LOC, altered mental status
  • neurologic signs; seizures, confusion, behavioural changes, cranial nerve palsies, focal neurological deficits, disorientation
  • more neurological symptoms than with meningitis
  • CSF lab values are the same for viral and bacterial meningitis
  • cultures, CSF analysis and serology used to diagnose
47
Q

What is the class clinical triad of encephalitis?

A
  • fever, headache, altered level of consciousness
48
Q

How is viral encephalitis transmitted?

A
  • usually access the brain through the bloodstream

Initial sites of infection:

  • respiratory tract (e.g. measles, mumps, varicella zoster)
  • gastrointestinal tract (e.g. poliovirus, enterovirus)
  • genital tract (e.g. HSV)
  • subcutaneous tissues (e.g. arbovirus such as West Nile)
49
Q

Why is viral encephalitis more serious than viral meningitis?

A
  • encephalitis is associated with higher intracranial pressures
50
Q

What is viral encephalitis caused by HSV?

A
  • most common cause of non-epidemic encephalitis
  • most infections caused by HSV-1 after neonatal period (especially > 50 years)
  • focal temporal lobe symptoms most common: visual field cut, hemiparesis, aphasia
  • Acyclovir shortens severity of illness
  • patients should be treated presumptively for HSV encephalitis until an alternate pathogen detected
  • otherwise, supportive therapy is used and sometimes corticosteroids
  • prognostic factors include age, duration of symptoms and Glasgow Coma Scale
  • not transmitted person-to-person
  • HSV dormant in the PNS ganglia until host factors are weakened; extremes of age
51
Q

What is viral encephalitis caused by West Nile Virus?

A
  • transmitted via infected mosquitoes into the bloodstream
  • causes body aches, meningitis, encephalitis, headache, fever, stiff neck, skin rash, coma, and even death
  • cannot be treated by Acyclovir, supportive therapy only
52
Q

What is a brain abscess?

A
  • focal intracerebral infection
  • pus containing cavity surrounded by inflamed tissue in the brain
  • 100% fatal prior to 1800s
  • mortality now 0-25% due to better antimicrobials, surgical techniques and imaging
  • difficult to sample, cause determined on context and history (ex. transplants, HIV, neutropenia, dental sepsis, trauma, etc.)
53
Q

What are the signs and symptoms of a brain abscess?

A
  • headache, mental status changes, focal neurological deficits, fever, clinical triad, seizures, N/V, nuchal rigidity, etc.
  • non-specific, related to increases in ICP but depends on the location of abscess and stage of infection
54
Q

How are brain abscesses diagnosed?

A
  • brain imaging
  • CT scan will show hypo-dense center with a peripherally uniform ring of enhancement following the injection of contrast material
  • CT guided aspiration can establish microbiologic diagnosis
  • surgical intervention can reduce pressure
55
Q

How are brain abscesses treated?

A
  • antimicrobial therapy detected at suspected organisms
  • empiric therapy narrowed when culture results available
  • aspiration or surgical excision of abscess if large
  • if origin of infection is identified, and the diameter of the abscess is less than 2.5 cm, can be treated without surgery
  • corticosteroids used in cases of increased ICP or significant edema

Introductory Microbiology (11 decks)

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