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Microbiology Exam V > Bacterial Infections of the CNS > Flashcards

Bacterial Infections of the CNS Flashcards

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1
Q

Entry of Pathogens (4 ways)

A

1) Hematogenous spread (e.g. Bacteremia)
2) Spread from a site adjacent to or contiguous with the CNS
3) Direct inoculation (e.g. head injury/fracture)
4) Neuronal Spread (usually from the peripheral nervous system)

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2
Q

Meningitis

A

1) Acute pyogenic –> think “neutrophils” –> Bacterial
2) Aseptic –> Viral
3) Chronic –> Any class of microbe

Bacterial is generally more sever and fatal than viral

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3
Q

Meningitis (Predisposing Factors)

A

1) Pneumococcal meningitis (Streptococcus pneumoniae)
- Pneumonia and Chronic Otitis Media

2) Meningococcal meningitis (Neisseria meningitidis)
- 10-20% of population are carriers
- History of recentl viral URTI
- Complement deficiencies (e.g. C6-9, Membrane Attack Complex)
- Outbreaks most common in winter (School and Miliatry Barracks)

Altered/Underdeveloped immune status puts you at increased risk of developing bacterial meningitis

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4
Q

Meningitis (Infectious Process)

A

1) Capsule (protects against phagocytic neutrophils and complement-mediated lysis)

2) Fimbriae, pilli, and outer membrane proteins
- Function in the colonization of nasopharynx, establishment of bacteremia, and attachment and penetration of the BBB

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5
Q

Meningitis (Pathophysiology)

A
  • Immune response to infection (INFLAMMATION) and damage caused by the bacterial agents (TOXINS) contribute to the pathophysiology
  • Bacterial toxins and cell wall components induce the production of inflammatory cytokines
  • Cytokines increase vascular permeability and transendothelial migration of immune cells (PMNs)
  • These events alter cerebral blood flow, intracranial pressure, alter composition of CSF, etc.

Edema/Intracranial Pressure/Seizures/Coma/DEATH

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6
Q

Meningitis (Diagnosis)

A

Approximately 50% of patients present with FEVER, HEADACHE, and STIFF NECK (nuchal rigidity)

  • Nearly 100% will present with a combination of 2 of the 4 following:
    1) Fever
    2) Headache
    3) Stiff Neck
    4) Altered Mental Status

Labs:

  • Gram stain of CSF
  • Cultures
  • Latex agglutination
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7
Q

Meningitis (Bacterial CSF Abnormalities)

A

1) Presence of PMNs NEUTROPHILS
2) Decreased Glucose
3) Increased Protein
4) Increased Pressure

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8
Q

Meningitis (Viral CSF Abnormalities)

A

1) Monocytes/Lymphocytes
2) RARE PMNs
3) Normal Glucose
4) Normal or slightly increased Protein and Pressure

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9
Q

Meningitis (Treatment)

A

1) Empiric Antibiotic Therapy
2) Age, predisposing factors, other symptoms may provide clues
3) Examination of CSF (gram stain) and results of latex agglutination testing of CSF may help dictate therapy

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10
Q

Meningitis (Infant Immunizations)

A 
Tetanus
Pertussis (Tdap)
Haemophilius influenzae type B (Hib)
Pneumococcal conjugate (PCV13)
Pneumococcal polysaccharide (PPSV23)
Meningococcal (Neisseria meningitidis)
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11
Q

Bacterial (Majority of Cases and Common Etiological Agents)

A

Majority of cases are in infants and children

Common Etiological Agents (All ages):

  • Strep pneumoniae (~50%)
  • Neisseria meningitides (~25%)
  • Group B Strep (~5-10%)- Strep agalactiae
  • Listeria monocytogenes (~5-10%)
  • Haemophilus influenzae (~5-10%)
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12
Q

What causes the majority of cases of bacterial meningitis in neonates?

A

Streptococcus agalactiae

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13
Q

What are the gram stain features of S. pneumonia, N. meningitidis, S. agalactiae (Group B Strep), L. monocytogenes, H. influenzae

A

S. pneumonia - Gram Positive Coccus, Alpha Hemolysis
N. meningitides - Gram Negative Coccus
S. agalactiae (Group B Strep) - Gram Positive Coccus
L. monocytogenes - Gram Positive Rod
H. influenzae - Gram Negative Short Rod

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14
Q

In what age groups do we worry about L. monocytogenes as a cause of bacterial meningitis?

A

Neonates (< 1 month) and the elderly

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15
Q

What are the most common causes of bacterial meningitis in infants, children, and adults?

A

Strep pneumoniae and Neisseria meningitides

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16
Q

Streptococcus pneumoniae (Characteristics)

A

Gram Positive Coccus
Grows in CHAINS (or DIPLOCOCCI in clinical specimens)
Oval or lancet-shaped cells
Polysaccharide CAPSULE (Virulent strains)
-Prevents against phagocytosis and complement-mediated lysis
-90 different capsular serotypes (each one elicits a different antibody response)
-Type-specific antibody is protective

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17
Q

Streptococcus pneumoniae (Lab Tests)

A

Catalase Negative
Round mucoid colonies on blood agar plates
Alpha hemolytic (green)
Distinguished from other alpha-hemolytic streptococci:
-Susceptibility to OPTOCHIN
-Susceptibility to BILE (Bile solubility test)

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18
Q

What is the most common cause of vaccine-preventable death in the U.S.?

A

Pneumococcal Disease

  • **common cause of bacterial meningitis among infants and young children
  • **increasing antibiotic resistance
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19
Q

Between 5 to 75% of the population is colonized with_______

A

Strep pneumoniae (more frequently in children than adults)

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20
Q

Pneumococcal Virulence Factors

A

Colonization of the oropharynx: binding of the choline-binding proteins of the bacterial cell wall to carbohydrates present on the surface of epithelial cells

Pneumolysin and an IgA protease prevent clearance from the respiratory tract (destroy ciliated epithelial cells/interefere with macrophage-mediated cleareance and degrade secretory IgA)

Thick Polysaccharide Capsule aids dissemination through the blood stream (interferes with phagocytic destruction by macrophages and neutrophils and protects from complement-mediated lysis)

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21
Q

Pneumococcal Meningitis

A 
Acute onset (generally hours)
High mortality (~30%)
Neurological sequela (10-20%) - i.e. permanent neurologic damage despite treatment
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22
Q

Pneumococcal Meningitis (Diagnosis)

A

Gram-stain of CSF
Latex-agglutination (detect presence of capsular antigens)

Longer tests –> cultivation, biochemical analysis, and susceptibility testing

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23
Q

Pneumococcal Meningitis (Treatment)

A

Emergency - initiate treatment without knowledge of the pathogen

Current recommendations:
-Vancomycin with a cephalosporin for 10-14 days
(Should be modified following identification and susceptibility testing)

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24
Q

Pneumococcal Meningitis Vaccine (PPV; PPV23)

A
  • Purified capsular polysaccharide antigen from 23 types of pneumococcus
  • Account for 88% of invasive pneumococcal disease
  • Cross-react with types causing additional 8% of disease

NOT effective in children <2 years old
60-70% effective against invasive disease
Less effective in preventing pneumococcal pneumonia

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25
Q

Pneumococcal Meningitis Vaccine (PPV; PPV23) (Recommendations)

A
  • Adults > or = 65 years of age
  • Persons > or = 2 years of age with: chronic illness, anatomic or functional asplenia, immunocompromised (disease, chemotherapy, steroids), HIV infection, environments or settings with increased risk
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26
Q

Pneumococcal Meningitis Vaccine (PCV13)

A

Pneumococcal polysaccharide conjugated to nontoxic diphtheria toxin
-13 capsular serotypes

Vaccine serotypes account for greater than 60% of invasive pneumococcal disease in children younger than 5

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27
Q

Pneumococcal Meningitis Vaccine (PCV7; PCV13)

A
  • Highly immunogenic in infants and young children
  • > 90% effective against invasive disease
  • Less effective against pneumonia (~70% reduction) and acute otitis media (~5% reduction)
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28
Q

Pneumococcal Meningitis Vaccine (PCV13) (Recommendations)

A
  • Routine vaccination of children

- Doses at 2, 4, 6, months, booster dose at 12-15 months

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29
Q

Neisseria meningitides (Characteristics)

A 
Gram Negative Diplococcus
Coffee or kidney bean appearance
Polysaccharide capsule (~12 serotypes)
Endotoxin referred to as lipooligosaccharide (LOS)
-Differs from LPS
-Shorter side chains
-No repeating polysaccharide
-Lipid A and core oligosaccharides similar to LPS
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30
Q

Neisseria meningitides (Labs)

A

Oxidase and Catalase Positive
Oxidizes both Glucose and Maltose (whereas, N. gonorrhoeae only oxidizes Glucose)
All Neisseria have fastidious growth requirements, often requiring atmosphere supplemented with CO2 for growth

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31
Q

Neisseria meningitides (Epidemiology)

A

Severe acute bacterial infection
Cause of meningitis, sepsis, and focal infections
Epidemic disease in sub-Saharan Africa “The Meningitis Belt”

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32
Q

What are the three most common clinical manifestations of N. meningitides (in order from most to least prominent)?

A

Meningitis (47.3%) > Bacteremia (43.3%) > Pneumonia (6.0%)

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33
Q

Neisseria meningitides (Pathology)

A

10% of population is COLONIZED
Transmission: aerosolized droplets
Outbreaks: most common where people are living in CLOSE CONTACT (e.g. households, barracks, schools, dorms)
>90% of cases of invasive meningococcal disease (Bacteremia and Meningitis) in the US are caused by one of five serotypes

34
Q

What are the five serogroups of Neisseria meningitides?

A 
C (32% of isolates)
B (24% of isolates)
Y (31% of isolates)
W-135 (6% of isolates)
A (< 1% of isolates)
35
Q

Which serotype is most common in children <2 years old?

A

50% of cases in <2 y.o. children are caused by Serogroup B

36
Q

Neisseria meningitides (Disease)

A 
1000-1500 cases of INVASIVE disease in US each year
Fatality rates: 10-15% (Highest in ADOLESCENTS)
Significant sequelae (NEUROLOGICAL DEFECTS, LIMB or DIGIT AMPUTATIONS) occurring in > or = 10% of infected individuals
37
Q

In which age groups are the two peaks of meningococcal disease seen?

A

Infants younger than 1 year old and young adults ages 15 to 24

38
Q

Meningococcal Disease

A

Incubation: 3-4 days (range 2-10 days)

Abrupt onset of fever, (meningeal symptoms) hypotension, and rash

39
Q

Meningococcal Virulence Factors

A

Pili (attaches to epithelial cells in nasopharynx)

Capsule (phagocytosis/complement-mediated lysis protection)

LOS (causes significant pathology –> Endotoxemia (organ failure) and DIC)

CNS entry facilitated by inflammatory response to infection (weakened BBB –> crosses BBB within neutrophils)

40
Q

Meningococcemia

A

Bloodstream infection
May occur with or without meningitis

Clinical Findings: Fever, Petechial/Purpuric Rash, Hypotension, Multiorgan Failure

41
Q

Meningococcal Meningitis

A

Result of HEMATOGENOUS DISSEMINATION

Clinical Presentation:
-Fever, Headache, Stiff Neck

42
Q

Meningococcal Meningitis (Diagnosis/Labs)

A

Clinical Signs and Lab Identification

Gram stain of CSF and/or blood
-Organisms are observable in the CSF and blood of ~75% of cases of meningitis

Patients with only Bacteremia
~30% have detectable organisms present in a peripheral blood smear (higher in BUFFY COAT preparation (WBCs))

Cultivation, biochemical analysis, and susceptibility testing achieve DEFINITIVE identification (however, take a long time)

Gram stain of lesion material (?)

Non-culture methods (Antigen detection in CSF; Serology)

43
Q

Meningococcal Meningitis (Treatment)

A

Penicillin

Empiric therapy with Vancomycin and a cephalosporin; however, once N. meningitides is confirmed, Penicillin alone is recommended

Treat family, classmates, co-workers prophylactically, as well

44
Q

Meningococcal Meningitis Vaccine (MPV; MPV4)

A

Tetravalent polysaccharide vaccine (A, C, Y, W-135)
Not effective in children <2 years of age, as it does not protect against the B serotype

Schedule: 1 dose with revaccination in 2-5 years (if indicated)

No booster response

Low affinity IgM, little IgG

45
Q

Meningococcal Polysaccharide Vaccine Recommendations

A

Not recommended for ROUTINE vaccination

Recommended for certain high-risk persons:

1) Terminal COMPLEMENT DEFICIENCY
2) Functional or anatomic ASPLENIA
3) Certain laboratory workers
4) Travelers to and U.S. citizens residing in countries in which N. meningitides is hyperendemic or epidemic (e.g. African Meningitis Belt)

46
Q

Meningococcal Polysaccharide Vaccine Recommendations (Outbreaks)

A

-Control of outbreaks
-Outbreak definition:
3 or more confirmed or probable cases
Period or = 10 cases per 100,000 population

47
Q

Meningococcal Conjugate Vaccine (MCV4)

A

-Licensed for use in individuals between the ages of 1 and 55

Tetravalent Vaccine (A, C, Y, W-135)

  • These serotypes account for 75% of all cases of invasive disease in children 11 to 18 years old (B is on the way)
  • Conjugated to non-toxic diphtheria toxin subunit*
48
Q

Meningococcal Conjugate Vaccine (MCV4) (Benefits)

A

Booster response observed
Higher affinity antibody response
Higher IgG response

49
Q

Which age groups are at the highest risk for Meningococcal disease?

A

College students living in dorms

In 2005, it was recommended that MCV4 vaccine be given to adolescents at their 11-12 year old visit, students entering high school (15 year olds), and college freshman living in dormitories

50
Q

Streptococcus agalactiae (GBS)

A 
Gram Positive Cocci
Grow in long CHAINS
Catalase Negative
Beta Hemolytic
Serologically classified Group B
Positive CAMP test
***Resistant to Bacitracin***
51
Q

Streptococcus agalactiae (GBS) (Epidemiology)

A

Over 1200 cases of GBS sepsis and meningitis in newborns annually
75% of cases occur during the FIRST WEEK OF LIFE (Early Onset Disease)
Infections occurring ONE TO THREE WEEKS AFTER BIRTH (Late Onset)
GBS causes more total infections in adults (sepsis, urinary tract infections, soft tissue infections)
-Incidence is much higher in neonates

52
Q

In which group is the highest incidence of invasive GBS found?

A

Black Neonates (< 1 year old) and Black Elderly (> 84 years old)

53
Q

Streptococcus agalactiae (GBS) Colonization/Carriers

A

MATERNAL COLONIZATION

  • Colonizes the lower GI tract and GU tract
  • Vaginal colonization has been reported in 10-30% of PREGNANT women
  • Maternal intrapartum GBS colonization is a MAJOR RISK FACTOR for the development of early onset disease in infants (>25% more likely to deliver infants with early onset GBS disease compared to women with no GBS colonization)
54
Q

Streptococcus agalactiae (GBS) (Virulence Factors)

A

Polysaccharide Capsule (resists phagocytosis and complement-mediated lysis)

Antibody-mediated opsonization appears to be protective; in the absence of maternal antibodies, the neonate is at risk

55
Q

Streptococcus agalactiae (GBS) (Risk Factors for Early-Onset GBS Disease)

A

Obstetric: prolonged rupture of membranes, preterm delivery, intrapartum fever
GBS bacteriuria during pregnancy
Previous infant with GBS disease
Demographic (African American race, Young age)
Immunologic (low antibody to GBS capsular polysaccharide)

56
Q

Streptococcus agalactiae (GBS) (Early-Onset Disease)

A
  • Bacteremia
  • Pneumonia
  • Meningitis (Respiratory distress, labored breathing, fever, lethargy, and irritability; Pneumonia may develop first and support suspicion of CNS involvement)
  • Mortality rate as high as 10% is observed
  • 25% of neonates who survive early onset disease suffer from PERMANENT NEUROLOGICAL SEQUELA (e.g. blindness, deafness, and mental retardation)
57
Q

Streptococcus agalactiae (GBS) (Late-Onset Disease)

A

Similar signs and symptoms
Meningitis is MORE COMMON
Survival rate is HIGHER
Neurological complications are MORE COMMON

58
Q

Streptococcus agalactiae (GBS) (Diagnosis)

A

-Recognition of clinical signs and the identification of the organisms
-Identification through:
Laboratory cultivation and biochemical analysis
…may be confirmed via serology to demonstrate the presence of Group B antigen

59
Q

Streptococcus agalactiae (GBS) (Treatment)

A

Penicillin

60
Q

Streptococcus agalactiae (GBS) (Prevention of Perinatal)

A

-Universal screening of all pregnant women between 35-36 weeks gestation
-Intrapartum antibiotics (Penicillin)
> or = 4 hours before delivery
Highly effective at preventing early-onset disease in women at risk of transmitting GBS to their newborns

61
Q

Streptococcus agalactiae (GBS) (Prevention of Neonatal)

A
  • Penicillin first-line agent for IAP (Ampicillin an acceptable alternative)
  • If culture results unknown at delivery, IAP if risk factors (fever, ROM > 18 hrs, preterm) present
  • Women with Bacteriuria during pregnancy or previous infant with GBS disease should receive IAP
62
Q

Haemophilus influenzae type B

A

Gram Negative Rod
Requires hemin (X) and NAD (V) for growth
Chocolate Agar
Polysaccharide Capsule (encapsulated strains)
-6 serotypes (a thru f)
-Type b = poly-ribitol phosphate (PRP) capsule
Prior to vaccination, 95% of all invasive disease was due to type B

63
Q

Haemophilus influenzae type B (Non-Encapsulated vs Encapsulated Strains)

A

Non-Encapsulated:

  • Pinkeye
  • Otitis Media
  • Sinusitis

Encapsulated Strains:

  • Meningitis
  • Epiglottitis
64
Q

Haemophilus influenzae type B (Hib Meningitis)

A

-Fever, stiff neck, headache
-Mortality is less than 5%, if treated
~25% of survivors experience PERMANENT NEUROLOGICAL SEQUELAE (e.g. hearing loss)

65
Q

Haemophilus influenzae type B (Diagnosis)

A

Gram stain of CSF

Latex agglutination test

66
Q

Haemophilus influenzae type B (Treatment)

A

Similar to other forms

Penicillin

67
Q

Haemophilus influenzae type B (Prevention)

A

Vaccination:

Non-conjugated Vaccine:

  • Poorly immunogenic in kids
  • No booster response (i.e. cell mediated immunity)

Conjugated

  • Anti-PRP antibodies
  • Highly immunogenic
  • Begin vaccinating at 2 months of age
  • Has reduced the incidence by ~95%
68
Q

Clostridium tetani - Tetanus

A

Gram Positive Rod
Anaerobic
Spore forming - terminal (“Drumstick”)
Produce a neurotoxin - Tetanospasmin

Spores common in soil and in feces of domestic animals

69
Q

Clostridium tetani - Tetanus (Pathogenesis)

A

Spores typically enter the body through wound contamination or traumatic inoculation

The umbilical stump can be contaminated, resulting in NEONATAL TETANUS

Following inoculation and under ANAEROBIC conditions, spores will germinate

Vegetative cells produce toxin

The toxin enters the bloodstream and enters the nervous system

70
Q

Clostridium tetani - Tetanus (Toxin)

A

A-B Toxin
B binds to motor neurons
Toxin is internalized and transported to spinal cord
Inactivates the release of inhibitory neurotransmitters
SPASTIC PARALYSIS

71
Q

Clostridium tetani - Tetanus (Signs and Symptoms)

A

Incubation of 2-10 days
Early signs include “lock jaw” (trismus), neck stiffness, difficulty swallowing, abdominal muscle rigidity
Followed by generalized muscle spasms, including severe back spasms
Death may occur due to Respiratory Failure

72
Q

Clostridium tetani - Tetanus (Diagnosis)

A

Symptoms may last for weeks and recovery may take months

Diagnosis is generally made based on CLINICAL PRESENTATION

  • Toxin is bound to neurons (difficult to detect)
  • Organism is difficult to grow
73
Q

Clostridium tetani - Tetanus (Treatment)

A 
Administer IMMUNOGLOBULIN (Passive Immunization)
Vaccinated with TETANUS TOXOID (Active Immunization)

Goal is to remove any unbound toxin

Clean wound/administer antibiotics to kill vegetative cells

Binding of toxin is IRREVERSIBLE - symptoms resolve as new axonal termini are generated

74
Q

Clostridium tetani - Tetanus (Prevention)

A

Vaccination with Tetanus Toxoid
The “T” in DTaP
Begin vaccinating at ~2 months
Booster shots every 10 years

75
Q

Clostridium botulinum - Botulism

A

Gram Positive Rod
Anaerobic
Spore forming - terminal
Produce neurotoxin - Botulinum Toxin

Spores:

  • Common in soil
  • Can contaminate meat, fish, veggies
  • Improperly canned food (Anaerobic environment)
  • Approximately 100 cases reported in the US annually
76
Q

Clostridium botulinum - Botulism (Disease)

A

Typically not an infect, but an INTOXICATION

  • Ingestion of PRE-FORMED TOXIN
  • Absorbed from gut to bloodstream

Infant Botulism - “Floppy Baby Syndrome”

  • Infants ingest food (honey) containing spores
  • Spores germinate in gut, produce
  • Accounts for 80% of cases in US annually
  • Tends to be MILDER in presentation
77
Q

Clostridium botulinum - Botulism (Toxin)

A 
***A-B Toxin***
B binds and A enters motor neurons
A blocks the release of Acetylcholine
Blocks stimulation
***FLACCID PARALYSIS***
78
Q

Clostridium botulinum - Botulism (Signs and Symptoms)

A

Symptoms develop within 12 to 72 hours of toxin ingestion
-Nausea, dry mouth, blurred vision, involuntary eye movement
-Muscle paralysis DESCENDS:
Ocular, Laryngeal, Respiratory, Respiratory, Trunk, Extremities

79
Q

Listeria monocytogenes

A 
Gram Positive Rod (Coccobacillus)
Motile - "Tumbling" motility in culture
Common in the environment
-Water and soil
-Feces/GI tract of many animals
Infection typically results from the consumption of contaminated food (e.g. milk, soft cheese, poultry)
80
Q

Listeria monocytogenes (Epidemiology)

A

5-10% of neonatal meningitis cases
5-10% of older adult cases

Common in immunosuppressed individuals and pregnant women
-Infection in utero can result in stillbirth, premature delivery

81
Q

Mycobacterium tuberculosis

A 
Primarily a disease of the lung
May spread to other sites
Infection of the CNS
-Meningitis
-Brain Abscess
-Most patients with meningitis have clinical historical evidence of pulmonary disease
-Chronic disease - develops SLOWLY
82
Q

Staphylococcus aureus

A

Meningitis - following bacteremia

Brain abscesses - traumatic inoculation or surgery

Microbiology Exam V (6 decks)

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