63/65-C. Diff and Meningitis Exemplar Flashcards

(58 cards)

1
Q

microbial exposure is constant

A

but clinical infection is rare

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2
Q

5 obligatory capabilities of microbes

A
attachment
spread
replication
evasion
transmission
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3
Q

risk of infection

A

dose*virulence
_____________
host resistence

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4
Q

dose

A

number of organisms

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5
Q

virulence

A

sum of organisms properties that help it cause infection

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6
Q

resistance

A

resistance of the host to infection, depending on anatomy and immune system

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7
Q

infection earlier in sequence

A

reliance on preformed effector molecules using non specific recognition molecules

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8
Q

infection later in sequence

A

synthesis of effector molecules, depends on specific recognition molecules

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9
Q

time for barrier

A

0-4 hours

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10
Q

time for innate

A

4-96 hours

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11
Q

time for adaptive

A

96+ hours

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12
Q

stages of infection

A
adherence
penetration
local infection
lymphatic spread
adaptive immunity
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13
Q

clinical reasoning

A

mechanisms
clinical presentation
context

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14
Q

inflammation in colon

A

increase mucous, peristalsis, bleeding

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15
Q

types of barriers

A

mechanical, physical, chemical, microbiome

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16
Q

epithelial cells

A

tight junctions, don’t leak

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17
Q

barriers to infection

A

non-specific
use preformed effector molecules so response is fast
use antimicrobial peptides (defensins)

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18
Q

chemical protection of gut

A

low pH
enzymes
antimicrobial peptides

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19
Q

antimicrobial peptides

A

defensins, cathelicidin, regIII

punch holes in bacterial membrane to kill

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20
Q

GI host defense

A
low pH, acidity
motility
mucous
bacterial colonization
GI mucosal immunity
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21
Q

GI mucosal immunity

A

sIgA and IgG
lymphoid follicles
Peyer’s patches
M cells

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22
Q

microbiome

A

all microbes, their genome, and environmental interactions

important for GI function and overall health

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23
Q

development of microbiology of GI tract

A

Sterile at birth
becomes colonized with maternal flora
initial colonization: aerobic (lactobacilli), create reducing environment
subsequent colonization: anaerobic

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24
Q

gut becomes colonized with commensal bacteria

A

mucosal becomes anti inflammatory

if infected it shifts to pro inflammatory

25
gut bacteria
outnumbers human cells 10x quantity varies along GI tract (more at end) Humans rely on gut bacteria
26
functions of gut bacteria
metabolic functions-breakdown sugars, produce vitamins | educate immune system
27
mucosa associated microbes
``` commensal symbionts bidirectional induction of gene expression (microbe influence human and vice versa) metabolism nutrition immune (anti inflammatory) ```
28
tight junctions
IL-10: anti inflammatory | IL-17: inflammatory, leaky
29
ID50
or organisms needed to cause disease in 50%
30
ID 50 in gut
lots needed for infection fewer needed if passed through skin barrier antibiotics clear microbiome and decrease ID50 by 30,000x
31
decrease ID 50
break barrier, antibiotics to clear microbiome, exposure to new bacteria
32
C. diff
lives as a spore | produce cytotoxins A and b
33
causes of C diff
old age Hospitalization medications - broad spectrum, proton pump inhibitors, chemotherapeutic drugs
34
4 forms of c diff
short term colonization acute diarrhea recurrent diarrhea fulminant diarrhea
35
symptoms of c diff
``` fever cramping adb pain bloody diarrhea fecal PMN ```
36
Antibiotics and c diff
disrupt microbiome
37
PPI and c diff
lower gastric pH so microbes can grow
38
chemotherapeutic agents
disrupt GI epithelium
39
treatment for c diff
fecal transplant | vancomycin or metronidazole
40
increase risk of GI infection
foods or meds that neutralize or reduce gastric acid secretion pernicious anemia gastrectomy
41
Petechiae
non blanching, tiny red spots | extravasation of blood from capillaries
42
purpura
large, dark irregular shaped lesions | significant bleeding into soft tissue
43
ecchymoses
coalesced purpura
44
left shift
marrow is stressed and releasing immature cells
45
n. meningitidis
gram negative coccus
46
structure of meningococcal cell wall
lipopolysaccharide for exotoxin pilus for attachment capsule with negative charge
47
pili
specific attachment to non ciliated nasopharyngeal cells or damage to ciliated cells
48
Lipopolysaccharide
LPS and CD14 form complex recognized by TLR and causes inflammation with NF-kB Cytokine release for T cell mediated immunity, B cell humoral immunity, or sepsis
49
hallmark of inflammation and infection
leukocytes and left shift
50
serum protein during inflammation
normal albumin>globulin | infection albumin
51
local inflammation in infection
increased permeability
52
systemic protective actions in infection
brain-fever liver-acute phase proteins bone marrow-leukocyte production (increase PMN, left shift)
53
systemic pathologic effects in inflammation
heart-low output, low BP (renal failure), increased o2 demand (hypoxia), acidosis blood vessel-increased permeability, vasodilation, leaky vessels, petechia and purpura
54
capsule on bacteria
fight with anticapsular antibody
55
greatest risk for bacterial meningitis
first 2 years of life
56
pure capsular vaccine
Ineffective before 2 years, shorter immunity, no memory t cells
57
conjugate vaccine
effective at all ages, longer immunity, recruits t cell memory
58
infection from capsulated organisms indicate
decreased antibodies decreased complement no spleen