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Neurology Micro > Bacterial Meningitis > Flashcards

Bacterial Meningitis Flashcards

1
Q

What are general things to know about bacterial meningitis?

A
  1. medical emergency
  2. acute onset and high mortality rate
  3. often irreversible damage to CNS
  4. S/sx: headache, vomiting, stiff neck, fever, photophobia, irritability
  5. ID of bacterial agents via CSF gram stain, RADT of capsular material in CSF, PCR testing, CSF and blood bacterial culture on non-selective media
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2
Q

What happens to the CSF w/ bacterial meningitis?

A
  1. large number of WBCs - especially PMN
  2. decreased glucose due to stress response
  3. elevated protein b/c of BBB breakdown
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3
Q

Common causes of bacterial meningitis in babies?

A

Group B strep
Gram negative enteric bacilli
Listeria monocytogenes

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4
Q

Common causes of bacterial meningitis in infants

A

Strep pneumonaie
N. Meningitis
H. Influzena type B

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5
Q

Common causes of bacterial meningitis in 2-18 yos

A

N. Meningitides

Strep Pneumonaie

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6
Q

Common causes of bacterial meningitis in ICPs

A

Staph spp
Gram negative enteri bacilli
Pseudomonas aeruginosa

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7
Q

Micro of Streptococci

A
  • Gram Positive found in either diplococci or long chains
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8
Q

types of Streptococci

A
  1. Strep Pneumonaie - aka pneumococcus, normal inhabitate of URT (40%), MCC of bacterial meningitis
  2. Strep Pyogenes - aka Group A strep, normal inhabitant of URT (15%), causes numerous local and systemic disease and post-disease sequelae
  3. Strep Agalactiae - Group B strep
  4. Viridans Streptococci - dental pathogen
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9
Q

How are the different Streptococci classified?

A
  1. Lancefield
  2. Capsular polysaccharides
  3. Biochemical rxns
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10
Q

What are lancefield antigens?

A

carbohydrate surface found in cell walls that determines the Lancefield groups A-H and K-U
- specificity based on amino sugar

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11
Q

Which of the streptococci uses Capsular polysaccharide

A

S. Pneumonaie

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12
Q

What types of diseases can Strep Pneumoniae cause?

A
  1. Pneumonia - usually lobar
  2. Bacteremia
  3. Otitis media - MC reason for antibiotic prescriptions in infants and kids
  4. Meningitis
    paranasal sinusitis, osteomyelitis, septic arthritis, endocarditis, peritonitis, cellulitis, and brain abscesses
    - currently the leading cause of invasive disease in kids, elderly, and ICPs
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13
Q

Pathogenesis of Strep Pneumoniae

A
  1. Colonization - adheres tightly to nasopharyngeal epithelium, may go to lungs or middle ear.
  2. Invasion - can alter vascular permeability to allow access to blood stream leading to lung infxns and bacteremia, can cross BBB by binding to cerebral capillaries, transmigrate and enter CSF to meningitis
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14
Q

How does strep pneumonia causes inflammation in middle ear

A

via pneumococcal cell wall components resulting in cytotoxicity on ciliated cell walls of cochlea

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15
Q

What are the virulence factors for Strep Pneumonia?

A
  1. Capsule - interferes w/ phagocytosis by binding to complement C3b. during invasion, encapsulated strains are 100,000 times more virulent
  2. Pili - used in initial event of invasion to adhere to URT
  3. Cell wall components - can create many symptoms of pneumonia, otitis media, and meningitis
  4. Choline Binding proteins - binds w/ carbs on pulmonary epithelial surface carbs. Important in crossing BBB during meningitis
  5. Hemolysins - pneumolysin lyses hose cells and activates complement
  6. H2O2 - damages host cells
  7. Neuraminidase and IgA protease - used in invasion of host tissues and destruction of secreted IgA at mucosal surface
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16
Q

Strep Pneumoniae vaccines

A
  1. Pneumovax

2. Prevnar

17
Q

Details of pneumonvax

A
  • multivalent, non-conjugated
  • use in older pts and high risk groups (HIV pts, transplant pts, cardiopulmonary pts, splenic disorders)
  • not effective in infants and young
  • immunity lats 5-7 years
18
Q

Details of prevnar

A
  • heptavalent, conjugated
  • safe but expensive
  • anamnestic response (adaptive immunity w/ memory)
  • can reduce meningitis by 85% in infants
19
Q

Micro details of N. Meningitides

A

Gram Negative
non-motile
diplococci
- may or may not have capsule

20
Q

What are the pathogenic Neisseria

A
  1. N. gonorrhoeae - STI, high prevalence, low mortality, only reservoir is humans
  2. N. Meningitidis - low prevalence, high mortality
21
Q

Virulence factor for N Meningitis

A

Prominent antiphagocytic polysaccharide capsule

- groupes on basis of the capsule - most important ones causing dz are A, B, C, Y, and W135

22
Q

Epidemiology of N Meningitidis

A
  • crowded conditions - day care centers, jails, military barracks
  • Sporadic outbreak - small number of related cases due to B, C, Y
  • Epidemic outbreak - large number of cases due to A
  • affects Sub-Saharan Africa
23
Q

Presentation of N Meningtidis

A
  • high mortality rate
  • begins abruptly w/ sudden high fever, stiff neck, chills, myalgias, weakness, N/V, headache
  • widespread petechial and purpuric skin lesions appear suddenly
  • apprehension, restlessness, and delirum
  • pulmonary insufficiency develops w/in a few hours,
    many pts die w/in 24 hours of being hospitalized
24
Q

Transmission of N. Meningitidis

A
  • Toxin = lipooligosaccharide = endotoxic
  • antiphagocytic capsule
  • Human nasopharynx is only reservoir and thus is spread via respiratory droplets and transmission requires aspiration of infective particles
  • invasion using pili and by a mechanism involving Phase Variation (turning off capsule genes) and then turning it on again once in bloodstream
25
Q

What is the treatment and control for N Meningitidis

A
  • Penicillin, chloramphenicol, 3rd gen cephalosporin is allergic to penicillin
  • Groups A, C, AC, and ACYW135 vaccines are available but ineffective in young kids
  • Group B capsule is homopolymer of sialic acid, not immunogenic in humans
26
Q

What are the vaccines for N. Meningitidis

A
  1. Menomune - for A, C, Y, W135. Unconjugated, used to control epidemics and for travelers to sub-saharan africa, cochlear transplant pts
  2. Menactra - for A, C, Y, and W135, Conjugated to toxoid, use in 11-55 year olds, recommended for all kids 11-12
    * neither vaccine covers serogroup B
27
Q

Pathogenesis of N. Gonorrhoeae

A

High frequency genetic variation

  1. Phase variation - changes in expression states of gene levels
  2. Antigenic variation - changes in genes leading to expression of different forms of similar genes
28
Q

What happens in phase variation?

A
  1. Direct DNA repeats
  2. Slipped strand mispairing
  3. Many systems use this - attachment proteins, capsule, invasion proteins, porin proteins, LPS/LOS, iron uptake proteins, restriction systems
29
Q

H. Influenzae common disease

A

otitis media, respiratory disease, and in young kids - meningitis

30
Q

Virulence factor for H. influenzae

A
  1. Polysaccharide capsule - serotype B is most important pathogen – anticapsular antibodies are protective but polysaccharide antigens are T cell dependent
31
Q

What is the current vaccine for H Influenzae

A
  • type B capsular polysaccharide (PRP) conjugated to carrier protein (diphtheria toxoid)
  • given to 2-15 month olds
32
Q

Why is there a low incidence of H. Influenzae

A

due to maternal antibodies

33
Q

Micro details of Listeria monocytogenes

A

Gram positive

Facultative IC parasite

34
Q

diseases caused by Listeria monocytogens

A
  • most infxns are Asx or mild flu like symptoms
  • meningitis and bacteremia can occur in ICPs, pregnancy women, and infants (due to vaginal colonization)
  • intrauterine infxn often kills fetus
35
Q

Reservoirs for Listeria monocytogenes

A

chickens, sheep, intestinal colonization, vaginal colonization

  • food borne transmission also important
  • killed by pasteurization but grows at refrigerator temperatures
36
Q

How does Listeria Monocytogenes invade

A
  • attaches and invades epithelial cells and macrophages
    1. endocytosis into non-phagocytic host cells mediated by internalin
  • then it spreads cell to cell avoiding exposure to humoral immune system
    2. Release from phagolysosome via listerolysin O
    3. F-actin bases motility
    4. Invasion of adjacent cell
    5. Bacterial replication
    6. cell death
37
Q

What does internalin do?

A

binds to E-cadherin expressed on epithelial cell surface

38
Q

What is necessary to kill Listeria Monocytogenes

A
  • cytokine activation of macrophages

Neurology Micro (6 decks)

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