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Immunology > 63/65-C. Diff and Meningitis Exemplar > Flashcards

63/65-C. Diff and Meningitis Exemplar Flashcards

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
Q

gut bacteria

A

outnumbers human cells 10x
quantity varies along GI tract (more at end)
Humans rely on gut bacteria

26
Q

functions of gut bacteria

A

metabolic functions-breakdown sugars, produce vitamins

educate immune system

27
Q

mucosa associated microbes

A 
commensal symbionts
bidirectional induction of gene expression (microbe influence human and vice versa)
metabolism
nutrition
immune (anti inflammatory)
28
Q

tight junctions

A

IL-10: anti inflammatory

IL-17: inflammatory, leaky

29
Q

ID50

A

or organisms needed to cause disease in 50%

30
Q

ID 50 in gut

A

lots needed for infection
fewer needed if passed through skin barrier
antibiotics clear microbiome and decrease ID50 by 30,000x

31
Q

decrease ID 50

A

break barrier, antibiotics to clear microbiome, exposure to new bacteria

32
Q

C. diff

A

lives as a spore

produce cytotoxins A and b

33
Q

causes of C diff

A

old age
Hospitalization
medications - broad spectrum, proton pump inhibitors, chemotherapeutic drugs

34
Q

4 forms of c diff

A

short term colonization
acute diarrhea
recurrent diarrhea
fulminant diarrhea

35
Q

symptoms of c diff

A 
fever
cramping 
adb pain
bloody diarrhea
fecal PMN
36
Q

Antibiotics and c diff

A

disrupt microbiome

37
Q

PPI and c diff

A

lower gastric pH so microbes can grow

38
Q

chemotherapeutic agents

A

disrupt GI epithelium

39
Q

treatment for c diff

A

fecal transplant

vancomycin or metronidazole

40
Q

increase risk of GI infection

A

foods or meds that neutralize or reduce gastric acid secretion
pernicious anemia
gastrectomy

41
Q

Petechiae

A

non blanching, tiny red spots

extravasation of blood from capillaries

42
Q

purpura

A

large, dark irregular shaped lesions

significant bleeding into soft tissue

43
Q

ecchymoses

A

coalesced purpura

44
Q

left shift

A

marrow is stressed and releasing immature cells

45
Q

n. meningitidis

A

gram negative coccus

46
Q

structure of meningococcal cell wall

A

lipopolysaccharide for exotoxin
pilus for attachment
capsule with negative charge

47
Q

pili

A

specific attachment to non ciliated nasopharyngeal cells or damage to ciliated cells

48
Q

Lipopolysaccharide

A

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
Q

hallmark of inflammation and infection

A

leukocytes and left shift

50
Q

serum protein during inflammation

A

normal albumin>globulin

infection albumin

51
Q

local inflammation in infection

A

increased permeability

52
Q

systemic protective actions in infection

A

brain-fever
liver-acute phase proteins
bone marrow-leukocyte production (increase PMN, left shift)

53
Q

systemic pathologic effects in inflammation

A

heart-low output, low BP (renal failure), increased o2 demand (hypoxia), acidosis
blood vessel-increased permeability, vasodilation, leaky vessels, petechia and purpura

54
Q

capsule on bacteria

A

fight with anticapsular antibody

55
Q

greatest risk for bacterial meningitis

A

first 2 years of life

56
Q

pure capsular vaccine

A

Ineffective before 2 years, shorter immunity, no memory t cells

57
Q

conjugate vaccine

A

effective at all ages, longer immunity, recruits t cell memory

58
Q

infection from capsulated organisms indicate

A

decreased antibodies
decreased complement
no spleen

Immunology (19 decks)

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