63/65-C. Diff and Meningitis Exemplar Flashcards Preview

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

Flashcards in 63/65-C. Diff and Meningitis Exemplar Deck (58)
1

microbial exposure is constant

but clinical infection is rare

2

5 obligatory capabilities of microbes

attachment
spread
replication
evasion
transmission

3

risk of infection

dose*virulence
_____________
host resistence

4

dose

number of organisms

5

virulence

sum of organisms properties that help it cause infection

6

resistance

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

7

infection earlier in sequence

reliance on preformed effector molecules using non specific recognition molecules

8

infection later in sequence

synthesis of effector molecules, depends on specific recognition molecules

9

time for barrier

0-4 hours

10

time for innate

4-96 hours

11

time for adaptive

96+ hours

12

stages of infection

adherence
penetration
local infection
lymphatic spread
adaptive immunity

13

clinical reasoning

mechanisms
clinical presentation
context

14

inflammation in colon

increase mucous, peristalsis, bleeding

15

types of barriers

mechanical, physical, chemical, microbiome

16

epithelial cells

tight junctions, don't leak

17

barriers to infection

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

18

chemical protection of gut

low pH
enzymes
antimicrobial peptides

19

antimicrobial peptides

defensins, cathelicidin, regIII
punch holes in bacterial membrane to kill

20

GI host defense

low pH, acidity
motility
mucous
bacterial colonization
GI mucosal immunity

21

GI mucosal immunity

sIgA and IgG
lymphoid follicles
Peyer's patches
M cells

22

microbiome

all microbes, their genome, and environmental interactions
important for GI function and overall health

23

development of microbiology of GI tract

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

24

gut becomes colonized with commensal bacteria

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