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Micro 7 > Bac CNS Infections > Flashcards

Bac CNS Infections Flashcards

1
Q

meningitis: two categories of CNS infections:

A
  • those which involve primarily the meninges (meningitis)

- those which are confined primarily to the brain parenchyma (encephalitis)

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2
Q

meningitis: in order to get in pathogens must …

A

get through/damage the blood brain barrier - PNS is NOT protected. Only CNS has

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3
Q

meningitis: entry of pathogens/where they come from:

A
  • Hematogenous spread from distant site of inoculation or infection.-bacteremia
  • Spread from a site adjacnt or contiguous with the CNS.
  • Direct inoculation.
  • Neuronal spread.
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4
Q

pyogenic think of….

A

PUS and NEUTROPHILS.. which means bacterial problem

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5
Q

aseptic menigitis is…

A

VIRAL - just how they named it

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6
Q

whats more severe meningitis?

A

bacterial is worse and more fatal than viral

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7
Q

predisposing factors meningitis

A

-URT bacteria
-UTI
-pneumonia and ottitis media
(Usualy neisserias)
-indiv with funky complement or missing completement
-dormitory/barracks/scools

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8
Q

infectious process meningitis

A
  • all organisms have a capsule to protect from destruction by neutrophils or complement
  • usually infections start somewhere else like URT
  • fimbriae pili and out membrane proteins= function in the colonization of the nasopharynx, the establishment of bacteremia and attachmen t and penetration of BBB
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9
Q

pathophysiology meningitis

A

-inflammation and toxins contribute –> but brain cant really swell bc in skull so that sucks –> so its damage by the bacteria and damage from inflammation

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10
Q

presentation/symptoms meningitis

A

fever, headache, stiff neck, altered mental status

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11
Q

labs/diagnosis meningitis

A
  • gram stain of CSF
  • cultures
  • latex agglutination - for bacterial antigens or DNA
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12
Q

Bacterial Meningitis

A
  • Presence of PMNs - neutrophils
  • Decreased glucose - bacteria consume it
  • Increased protein
  • Increased pressure
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13
Q

Viral Meningitis / Encephalitis

A
  • Mono/Lymphos - no neutrophils
  • Rare PMNs
  • Normal glucose
  • Normal or slightly increased protein and pressure
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14
Q

treatment bacterial meningitis

A
  • usually antibiotic therapy is started so pt does die

- look at stain and latex agglut results

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15
Q

bacterial meningitis - nmajor organisms and group most infected

A
  • S. pneumoniae (~50%) - (OLD FOLKS)
  • N. meningitides (~25%)
  • Group B Strep. (~5-10%) – S. agalactiae (VERY YOUNG KIDS)
  • Listeria monocytogenes (~5-10%) - VERY OLD MOSTLY AND SOME YOUNG
  • Haemophilus influenzae (~5-10%)

-mostly infants and children

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16
Q

neonates (<1mo) most common bacterial meningitis orgs

A
  • GROUP B STREP**
  • E Coli
  • other gram neg enterics
  • listeria monocytogenes*
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17
Q

infants (<2mo) most common bacterial meningitis orgs

A
  • S Pneumo

- neisseria meningitidis

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18
Q

Children (2-18yrs) most common bacterial meningitis orgs

A
  • n meningitidis

- S pneumo

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19
Q

adults (>18yrs) most common bacterial meningitis orgs

A
  • S pneuomo
  • n meningitidis
  • listeria monocytogenes***
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20
Q

Streptococcus pneumoniae features:

A
  • gram pos coccus (sometimes diplococcus)
  • grows in chains
  • catalase neg
  • oval or lancet shaped cells
  • polysaccharide capsule (90 types and type specific antibody is protective)
  • susceptible to optochin
  • susceptible to bile (bile solubility)
  • ALHPA HEMO (GREEN)
  • round mucoid colonies on blood agar
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21
Q

most common vaccine-preventable disease?

A

pneumococcal disease

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22
Q

pneumococcal virulence factors:

A
  • to colonize oropharynx = choline binding proteins of bact cell wall bind carbs on epithelial cells
  • Pneumolysin and IgA protease prevent clearange by destroying ciliated epith cells and degrading secreted IgA
  • thick polysaccharide capsule to get through blood stream - protect from macrophag and complement destruction
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23
Q

symptoms of acute bacterial meningitis (includes pneumococcal)

A

-fever, headache, stiff neck

sometimes altered mental status

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24
Q

pneumococcal meningitis diagnosis

A
  • Recognize clinical signs and lab identification
  • Gram-stain of CSF
  • Latex-agglutination
  • detect the presence of capsular antigens
  • Cultivation, biochemical analysis, and susceptibility testing achieve definitive identification and guide treatment
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25
Q

pneumococcal meningitis - treatment

A

vancomycin with a cephalosporin
therapy should be modified following identification and susceptibility testing.
Treat for 10-14 days.

-usually not penicillin (resistance)

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26
Q

pneumococcal meningitis - vaccine

A
  • started as a 23 valent polysaccharide conjugate vaccine-Did not work well in young kids – they have trouble with the polysacch conjugate
  • now we have a 13 valent polysaccharide conjugated to diphtheria toxin
  • all children 2, 4, 6 month shots with booster at 12-15 months
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27
Q

Neisseria meningitidis - organism details

A
  • gram neg diplococcus
  • coffee or kidney bean appearance
  • polysaccharide capsule
  • endotoxin=LOS- NOT LPS
  • oxidase pos
  • catalase pos
  • oxidizes glucose and maltose (MALTOSE POS)
  • needs CO2 for growth
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28
Q

LOS vs LPS

A
  • LOS has shorter side chain
  • no repeating polysacch
  • lipid A and oligosacchs are similar
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29
Q

neisseria meningitdis - transmission?

A

-aerosolized droplet - respiratory

30
Q

neisseria meningitdis - clinical/symptoms

A
  • abrupt onset of fever, hypotension and rash
  • stiff neck
  • multi organ failure
  • entry into CNS is usually facilitated by inflammatory resomnse to infection - moves into brain INSIDE NEUTROPILS
31
Q

neisseria meningitdis - virulence factors

A
  • pili - attach to epith in nasopharynx
  • capsule: prevent phagocytosis and complement
  • LOS - endotoxemia = organ failure
32
Q

neisseria meningitdis - diagnosis

A
  • Recognize of 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
  • Can use antigen detection in CSF and serology
33
Q

neisseria meningitidis - treatment

A
  • quickly- vancomyocin/cephalosporin
  • if neisseria m is CONFIRMED use peniciillin
  • treat family/close others too
34
Q

neisseria meningitidis - vaccine

A

tetravalent - polysacch conjugate (to non toxic diphtheria toxin subunit) vaccine (A,C,Y,W-135)

  • doesnt protect against B-serotype
  • 1 dose with revaccination in 2-5 years
  • not effective in the very young <2yrs
35
Q

Streptococcus agalactiae (GBS) organism details

A
  • Gram-positive cocci
  • Grow in long chains
  • Catalase negative
  • Beta-hemolytic
  • Serologically classified Group B. –> HITS NEONATES HARD
  • Positive CAMP test
  • Resistance to bacitracin
36
Q

Streptococcus agalactiae (GBS) mostly affects:

A

NEONATES 1-3weeks after birth

37
Q

major risk factor for neonates developing group b strep strep agalactiae meningitis?

A
  • colonizes the vagina in some pregnant women (also lower GI and genitourinary
  • need to test women for this to reduce risk
  • histroy of UTI
  • premature baby
  • longer time in delivery from water breakage to baby out
38
Q

Streptococcus agalactiae (GBS) - virulence factors

A
  • polysacch capsule - complement and phago stuff

- antibody mediated opsonization appears to be protective

39
Q

Streptococcus agalactiae (GBS) - early onset meningitidis

A
  • first week of life
  • respiratory distress, labored breating, fever, lethargy, irritability
  • pneumonia may develop first
40
Q

Streptococcus agalactiae (GBS) - late onset meningitidis

A
  • after first week of life
  • neurological complications more common
  • better survival rate
41
Q

Streptococcus agalactiae (GBS)- diagnosis

A
  • Recognition of clinical signs and the identification of the organisms (lethary, fever)
  • Identification through laboratory cultivation and biochemical analysis - confirm via seroloy to confimr presence of group b antigen
42
Q

Streptococcus agalactiae (GBS)- treatment

A

-penicillin

43
Q

Streptococcus agalactiae (GBS)- prevention

A
  • screen all pregant women between 35-36weeks

- if they have start inpartum antibiotis (penicillin)

44
Q

Haemophilus influenzae type B - organism details;

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
45
Q

Haemophilus influenzae non encapsulated strains infect:

A
  • Pinkeye
  • Otitis Media
  • Sinusitis
46
Q

Haemophilus influenzae -encapsulated strains infect;

A
  • Meningitis

- Epiglottitis

47
Q

Haemophilus influenzae - symptoms

A

fever
stiff neck
headache
altered mentals tatus

48
Q

Haemophilus influenzae - diagnosis

A
  • Gram-stain of CSF

- Latex agglutination test

49
Q

Haemophilus influenzae - treatment:

A

antibiotics - probs penicillin or ampicillin cephalosporin… that shit

50
Q

Haemophilus influenzae - vaccine

A

-CONJUGATED
-Anti-PRP antibodies
Highly immunogenic
Begin vaccinating as 2 months of age
Has reduced the incidence by ~95%

51
Q

15 year old with gram neg cocci youre thinking:

A

neisseria m

52
Q

15 year old girl with gram pos cocci youre thinking?

A

strep pneumo

53
Q

15 hour old kid with gram pos cocci

A

group B strep - strep agalactiae

54
Q

what if positive india ink stain?

A

strep neoformans

55
Q

Clostridium tetani - tetanus - organism details

A
  • Gram-positive rod
  • Anaerobic
  • Spore forming – terminal (“drumstick”)
  • Produce a neurotoxin – tetanospasmin
56
Q

clostridium tetani found in?

A

spores found in soil and feces of domestic animals

57
Q

typical way clostridium tetani infects and how it affects tissues?

A
  • wound contamination or umbilical stump contamination in fetus with spores
  • spores germinate under anaerobic conditions (deep in tissues)
  • vegetative cells produce toxin
  • toxin enters the blood stream and enters teh nervous system
58
Q

clostridium tetani - what kind of toxin produces and what kind of effect?

A
  • A-B toxin - A- attaches - B-does the harm once in
  • B binds to motor neurons - IIRREVERSIBLY - Recovery means that you need to regenerate new axon termini
  • Toxin is internalized and transported to spinal cord.
  • Inactivates the release of inhibitory neurotransmitters.
  • SPASTIC PARALSIS
59
Q

clostridium tetani - early signs and progression

A
  • Early signs include “lock jaw” (trismus), neck stiffness, difficulty swallowing, abdominal muscle rigidity.
  • Followed by generalized muscle spasms, including severe back spasms.
  • Spasms grow more frequent and can last several minutes
  • Death may occur due to reparatory failure
  • Symptoms last weeks
60
Q

clostridium tetani - diagnosis

A
  • generally made based on clinical presentation.
  • Toxin is bound to neurons (difficult to detect)
  • Organism is difficult to grow.
61
Q

clostridium tetani - treatment

A
  • Administer immunoglobulin (passive immunization)
  • Vaccinated with tetanus toxoid (active immunization)
  • The goal is to remove any unbound toxin !)
  • Clean wound and administer antibiotics to kill vegetative cells.
  • supportive therapy as needed.
  • may take months to recover
62
Q

clostridium tetani - vaccine

A
  • tetanoid toxoid used
  • begin vaccination at 2 yrs
  • booster every 10 years
63
Q

Clostridium botulinum - Botulism - organism details

A
  • Gram-positive rod
  • Anaerobic
  • Spore forming – terminal - found in soil, contaminate meat fish veggies, canned food, HONEY
  • Produce neurotoxin – botulinum toxin
64
Q

Clostridium botulinum - infects how?

A

-ingestion of preformed toxin (INTOXICATION)

65
Q

clostridium botulinum- what kind of toxin produces and what kind of effect?

A 
A-B toxin
B binds and A enters motor neurons
A blocks the release of Acetycholine
Blocks stimulation
FLACCID PARALYSIS
66
Q

clostridium botulinum - symptoms:

A
  • Nausea, dry mouth, blurred vision, involuntary eye movement
  • paralysis desceds DOWNWARD from head
67
Q

Listeria monocytogenes - organism detail:

A
  • Gram-positive rod (coccobacillus)

- Motile (“tumbling” motility in culture)

68
Q

Listeria monocytogenes where is it found that infects?

A
  • water and soil
  • feces of animals
  • consumption of contaminated food: milk, soft chesse, poultry
69
Q

Listeria monocytogenes where is it seen population wise?

A

very young and very old

-immunosuppressed and pregos

70
Q

Mycobacterium tuberculosis - how does it infect?

A

prmarily starts in lung but spreads to the CNS - results in: meningitis
brain abscess
Most patients with meningitis have clinical of historic evidence of pulmonary disease
Chronic disease – develops slowly

71
Q

Staph aereus - meningitidis

A

-follows bacteremia

results in brain abcesses-

Micro 7 (6 decks)

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