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)
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
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.
4
Q
pyogenic think of….
A
PUS and NEUTROPHILS.. which means bacterial problem
5
Q
aseptic menigitis is…
A
VIRAL - just how they named it
6
Q
whats more severe meningitis?
A
bacterial is worse and more fatal than viral
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
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
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
10
Q
presentation/symptoms meningitis
A
fever, headache, stiff neck, altered mental status
11
Q
labs/diagnosis meningitis
A
- gram stain of CSF
- cultures
- latex agglutination - for bacterial antigens or DNA
12
Q
Bacterial Meningitis
A
- Presence of PMNs - neutrophils
- Decreased glucose - bacteria consume it
- Increased protein
- Increased pressure
13
Q
Viral Meningitis / Encephalitis
A
- Mono/Lymphos - no neutrophils
- Rare PMNs
- Normal glucose
- Normal or slightly increased protein and pressure
14
Q
treatment bacterial meningitis
A
- usually antibiotic therapy is started so pt does die
- look at stain and latex agglut results
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
16
Q
neonates (<1mo) most common bacterial meningitis orgs
A
- GROUP B STREP**
- E Coli
- other gram neg enterics
- listeria monocytogenes*
17
Q
infants (<2mo) most common bacterial meningitis orgs
A
- S Pneumo
- neisseria meningitidis
18
Q
Children (2-18yrs) most common bacterial meningitis orgs
A
- n meningitidis
- S pneumo
19
Q
adults (>18yrs) most common bacterial meningitis orgs
A
- S pneuomo
- n meningitidis
- listeria monocytogenes***
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
21
Q
most common vaccine-preventable disease?
A
pneumococcal disease
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
23
Q
symptoms of acute bacterial meningitis (includes pneumococcal)
A
-fever, headache, stiff neck
sometimes altered mental status
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
25
pneumococcal meningitis - treatment
vancomycin with a cephalosporin
therapy should be modified following identification and susceptibility testing.
Treat for 10-14 days.
-usually not penicillin (resistance)
26
pneumococcal meningitis - vaccine
- 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
27
Neisseria meningitidis - organism details
- 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
28
LOS vs LPS
- LOS has shorter side chain
- no repeating polysacch
- lipid A and oligosacchs are similar
29
neisseria meningitdis - transmission?
-aerosolized droplet - respiratory
30
neisseria meningitdis - clinical/symptoms
- 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
neisseria meningitdis - virulence factors
- pili - attach to epith in nasopharynx
- capsule: prevent phagocytosis and complement
- LOS - endotoxemia = organ failure
32
neisseria meningitdis - diagnosis
- 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
neisseria meningitidis - treatment
- quickly- vancomyocin/cephalosporin
- if neisseria m is CONFIRMED use peniciillin
- treat family/close others too
34
neisseria meningitidis - vaccine
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
Streptococcus agalactiae (GBS) organism details
- 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
Streptococcus agalactiae (GBS) mostly affects:
NEONATES 1-3weeks after birth
37
major risk factor for neonates developing group b strep strep agalactiae meningitis?
- 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
Streptococcus agalactiae (GBS) - virulence factors
- polysacch capsule - complement and phago stuff
| - antibody mediated opsonization appears to be protective
39
Streptococcus agalactiae (GBS) - early onset meningitidis
- first week of life
- respiratory distress, labored breating, fever, lethargy, irritability
- pneumonia may develop first
40
Streptococcus agalactiae (GBS) - late onset meningitidis
- after first week of life
- neurological complications more common
- better survival rate
41
Streptococcus agalactiae (GBS)- diagnosis
- 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
Streptococcus agalactiae (GBS)- treatment
-penicillin
43
Streptococcus agalactiae (GBS)- prevention
- screen all pregant women between 35-36weeks
| - if they have start inpartum antibiotis (penicillin)
44
Haemophilus influenzae type B - organism details;
- 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
Haemophilus influenzae non encapsulated strains infect:
- Pinkeye
- Otitis Media
- Sinusitis
46
Haemophilus influenzae -encapsulated strains infect;
- Meningitis
| - Epiglottitis
47
Haemophilus influenzae - symptoms
fever
stiff neck
headache
altered mentals tatus
48
Haemophilus influenzae - diagnosis
- Gram-stain of CSF
| - Latex agglutination test
49
Haemophilus influenzae - treatment:
antibiotics - probs penicillin or ampicillin cephalosporin... that shit
50
Haemophilus influenzae - vaccine
-CONJUGATED
-Anti-PRP antibodies
Highly immunogenic
Begin vaccinating as 2 months of age
Has reduced the incidence by ~95%
51
15 year old with gram neg cocci youre thinking:
neisseria m
52
15 year old girl with gram pos cocci youre thinking?
strep pneumo
53
15 hour old kid with gram pos cocci
group B strep - strep agalactiae
54
what if positive india ink stain?
strep neoformans
55
Clostridium tetani - tetanus - organism details
- Gram-positive rod
- Anaerobic
- Spore forming – terminal (“drumstick”)
- Produce a neurotoxin – tetanospasmin
56
clostridium tetani found in?
spores found in soil and feces of domestic animals
57
typical way clostridium tetani infects and how it affects tissues?
- 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
clostridium tetani - what kind of toxin produces and what kind of effect?
- 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
clostridium tetani - early signs and progression
- 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
clostridium tetani - diagnosis
- generally made based on clinical presentation.
- Toxin is bound to neurons (difficult to detect)
- Organism is difficult to grow.
61
clostridium tetani - treatment
- 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
clostridium tetani - vaccine
- tetanoid toxoid used
- begin vaccination at 2 yrs
- booster every 10 years
63
Clostridium botulinum - Botulism - organism details
- Gram-positive rod
- Anaerobic
- Spore forming – terminal - found in soil, contaminate meat fish veggies, canned food, HONEY
- Produce neurotoxin – botulinum toxin
64
Clostridium botulinum - infects how?
-ingestion of preformed toxin (INTOXICATION)
65
clostridium botulinum- what kind of toxin produces and what kind of effect?
```
A-B toxin
B binds and A enters motor neurons
A blocks the release of Acetycholine
Blocks stimulation
FLACCID PARALYSIS
```
66
clostridium botulinum - symptoms:
- Nausea, dry mouth, blurred vision, involuntary eye movement
- paralysis desceds DOWNWARD from head
67
Listeria monocytogenes - organism detail:
- Gram-positive rod (coccobacillus)
| - Motile (“tumbling” motility in culture)
68
Listeria monocytogenes where is it found that infects?
- water and soil
- feces of animals
- consumption of contaminated food: milk, soft chesse, poultry
69
Listeria monocytogenes where is it seen population wise?
very young and very old
| -immunosuppressed and pregos
70
Mycobacterium tuberculosis - how does it infect?
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
Staph aereus - meningitidis
-follows bacteremia
| results in brain abcesses-
