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Anderson Immunology/Microbiology Flashcards

1
Q

normal flora: acid tolerant organisms in stomach
normal flora: anaerobic bacteria of small intestine
normal flora: lg intestine

A

stomach: lactobacilli, streptococci
sm intestine: parasites, fungi
lg intestine: bifidobacter, eubacter, enterobacter, peptostreptococci

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2
Q 
anterior urethra normal flora
vagina
skin
nose
conjunctiva
A

ant urethra: lactobacilli, cornybacteria, coag - staph

vagina: lactobacilli (staph, strep)
skin: staph, candida, clostridia, acinetobacteria
nose: anaeorobes
conjunctiva: coag - staph

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3
Q

principles of infectious disease

A

attachment
replication
spread
shedding/elimination

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4
Q

how does body respond to viral vs bacterial infections

A

viral: lymphocytes go up and neuts (PMNs) go down
chronic virus: decreased lymphocytes
bacterial: neuts (PMNs) go up and lymphocytes go down and increased band cells (immature cells)
chronic bacterial: decreased neuts and increased monocytes

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5
Q

fungal infections

A

delayed hypersensitivity reaction

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6
Q

tumors

A

t-cell response to tumor growth

activate NKs and macrophages

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7
Q

*compare and contrast endo and exotoxins

A

endo: LPS, part of outer membrane, not denatured by boiling, antigenic, don’t form toxoid, low potency, cause fever
exo: protein, diffusible (extracellular), denatured by boiling, antigenic, form toxoid, high potency, sometimes cause fever

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8
Q

hypothalamic set-point for body temp

A

temp sensors in skin and hypothalamus read core temp and tell anterior hypothalamus.
ant hypothalamus tells other body systems to heat up or cool down body.

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9
Q

what increases the set-point of temperature?

A

pyrogens

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10
Q

what are the heat-generating mechanisms?

heat loss mechanisms

A
  • increased metabolism, shivering, vasoconstriction (post hypothalamus)
  • vasodilation, increased sympathetic outflow to sweat glands (post hypothalamus)
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11
Q

how does body respond to viral infection?

A

proliferation of lymphocytes and reduction of PMNs
NK and cytotoxic cells
IgG/IgM neutralize viral particles in blood
interferon

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12
Q

chronic viral infection

A

can result in reduced # of circulation lymphocytes

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13
Q

bacterial infections

A

PMNs (neutrophils) increase and lymphocytes decrease

see band cells

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14
Q

fungal infection causes what type of response

A

type 1 IgE response

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15
Q

response to tumors

A

t-cell response
NK cells
macrophages

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16
Q

endotoxin vs exotoxin

A

endotoxin: LPS in outer membrane, not denatured by boiling, pyrogenic
exotoxin: protein extracellular, denatured by boiling, form toxoid, high potency

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17
Q

non-specific immunity

A

physical barrier: skin, mucus membranes, gastric acid and enzymes

physiological barriers: inflammation, phagocytosis (macrophages, monocytes, PMNs, eosinophils, cell death = pus)

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18
Q

which are granular and which are agranular WBCs?

A

granular: neutrophils, basophils, eosinophils (phils)
agranular: moncytes and lymphocytes

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19
Q

what causes heat (heat generation)

A

thyroid hormone
cold temperature activates sympathetic
shivering (rigors is body trying to raise temperature)

heat loss mechanisms (want to stop if cold and promote if hot): radiation, convection, evaporation

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20
Q

hypothalamic set point

A

thermosensors in hypothalamus keep track of temp
belief of what temp should be (98.6)

  • too low: heat generating
  • too high: heat loss
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21
Q

pyrogens

A

increase set point temp
core temp recognized as lower than the new set-point temp by ant hypothalamus
induce cytokines

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22
Q

what is the trigger for fever?

A

Interleuken 1 IL-1

pyrogens cause reaction that causes body to dump out IL-1
IL-1 goes to hypothalamus and tells prostaglandins to increase temp

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23
Q

how does aspirin reduce fever?

A

inhibits cyclooxygenase which inhibits production of prostaglandins and decreases set point

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24
Q

heat exhaustion vs heat stroke

A

heat exhaustion: caused by excessive sweating. Decreased blood volume and BP. Wet, exhausted, fainting

heat stroke: occurs when body temp increases to point of tissue damage. Core temp increases. Dry, can’t perspire, brain can shut off and die.

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25
Q

NK cells

A

non-specific
cytotoxic cells
create hole in ag cell and kill it
stimulated by complement cascade

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26
Q

specific immunity

A

fetal stem cells mature to t-cells in thymus

t and B cells hang out in lymph nodes and wait for an ag to come through

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27
Q

everything matures in ____ except for ____ which mature in the ____

A

bone marrow
t-cells
thymus

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28
Q

all antibodies come from

A

B cell response

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29
Q

myeloid stem cells become what?

A

magakaryocyte -> platelets
proerythroblast -> Reticulocytes -> RBCs
monoblast -> WBCs
myeloblast

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30
Q

what do lymphoid stem cells make

A

t-cells

cell mediated immunity (kill other tissues or cells)

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31
Q

humoral immunity

A

cells that produce ab that inactivate invader

NK cells (just kill)

32
Q

full response to ag

A

APCs present ag to t-cells
t-cells stimulate b-cells while attacking ag
B cells produce ab
ab attacks ag

33
Q

monocytes vs macrophages

A

mono in blood
mac in tissue

  • both are phagocytic
34
Q

complement

A

activation of endogenous proteins in case of immunologic need.

classical pathway: ag activates = ag/ab reaction
alternate pathway: activates compliment cascade in middle (at C3 locus) without ag/ab reaction. less effective

35
Q

Interferon

A

released from cells when they are infected

  • go tell other cells that there is an invader
  • other cells produce anti-viral enzymes

alpha interferon: activates NK

beta: growth
gamma: NK, t-cells, macrophages

36
Q

TNF

A

immune stimulating cytokine
extrinsic pathway for triggering apoptosis.
tumor necrosis factor = TNF alpha

37
Q

IL - 1

A

triggers fever

secreted by macrophages and monocytes

38
Q

MHC 1 and MHC 2

major histocompatability complexes

A

MHC 1: help CD 8 t-cells recognize and target virally infected and cancer cells

MHC 2: help CD 4 t helper cells dock on macrophage

39
Q

CD 8 T cells

A

cytotoxic: attack and destroy infected cells

memory t-cells: await reappearance of ag

suppressor t-cells: control or modulate immune response by T cells and B cells

40
Q

CD 4 T-cells

A

helper t-cell: stimulate immune response by t-cells and b-cells. tell B cells to make ab

memory t helper cells: await reappearance of ag. Tell B cells to make more ab

41
Q

first response immunoglobulin

A

IgM

42
Q

primary and secondary response in humoral immunity

A

B-cell mediated

primary: interleukins, prostaglandins, TNF, IFN, adherence proteins are released
secondary: Ig’s produced (IgM still there, but IgG is immediate and large quantity. specific

43
Q

IgA

A

secretory
tears, saliva, mucus
prevents bacteria, viruses, toxin from attaching

44
Q

IgE

A

allergy
type-1 immediate hypersensitivity
parasite infection

45
Q

IgM

A 
first responder
short time period
B cells produce IgM
elevated in acute infection 
basis for ABO blood type
no false positives
46
Q

IgG

A 
Long term
most common
focuses NK to their targets
passive immunization (gamma globulin injection)
crosses placenta
47
Q

type-1 hypersensitivity reaction

A

IgE mediated

anaphylaxis

48
Q

Type II hypersensitivity

A

ab mediated response

Goodpastures: antiglomerular and antialveolar ab

49
Q

Type III hypersensitivity

A

ab/ag complexes
immune complex mediated
serum sickness (reaction to other blood in system)

50
Q

Type IV hypersensitivity reaction

A

non- ab
t-cell mediated
TB skin test reaction

51
Q

Autoimmunity ab reaction

A

can happen with any hypersensitivity reaction

52
Q

autoimmune diseases: DiGeorge’s syndrome

A

thymic hypoplasia
total absence of cell mediated immunity
agenesis of third and fourth pharyngeal pouches

53
Q

Scleroderma/Systemic Sclerosis

A

autoimmune
excessive collagen
fibrosis in microvasculature: skin, GI, kidneys, heart, lungs
mask-like face

54
Q

Lupus (SLE)

A

autoimmune injury to skin, kidney, serosal membranes
febrile illnesses
type III hypersensitivity

55
Q

HIV

A

immunosuppression
infect CD4 T cells
CD 8 do job, but CD 4 can’t help so no B cells either
infection of monocytes and macrophages

56
Q

beta hemolysis vs alpha hemolysis

A

beta: complete, more of a problem
alpha: partial

57
Q

gram positive cocci staph aureus

A 
staph aureus 
clusters 
beta hemolytic
coagulase positive
empitigo
tts
scalded skin sydrome
osteomyelitis
58
Q

staph food poisoning

A

enterotoxin
toxin release form ingested staph
4 hours after ingestion
true food poisoning from toxin not staph itself

59
Q

staph epidermidis

A

coagulase neg
surgical wound infections
subacute endocarditis

60
Q

staph saprophyticus

A

not common
coag neg
UTIs (community aquired)

61
Q

everyone at dinner party at food that caused it staph aureus food poisoning. Which food caused it?

A

not cooked or kept cold (bug stays alive at room temp)

62
Q

Group A beta hemolytic strep

Group B beta hemolytic strep

A

catalase negative chains
A: strep through, pharyngitis, scarlett fever, rheumatic fever

B: vaginal infections, neonatal

63
Q

Group D strep

A

enterococci: URIs and needle sticks

S pneumoniae: pneumonia, sinusitis, otitis media, meningitis

s. viridans: dental work, endocarditis, bacteremia

64
Q

How does n. gonorrhea avoid specific immune system?

A

cilia to attach to mucus membranes

anti-human IgA so IgA can’t attack it

65
Q

N meningitidis

and sx

A

catalase and oxidase positive
100% fatal if not treated
fever, ha, nuchal rigidity, purpura
infants: no nuchal rigidity, GI symptoms

66
Q

Waterhouse friedrichsen syndrome

A

N. meningitidis -> menigococcemia -> waterhouse friedrichson -> high fever, DIC, adrenal destruction

67
Q 
most likely organism for meningitis:
0-4 weeks: 
4-12 weeks
3 months - 18 years
18 - 50
>50
A 
0-4 weeks: Group B strep, E. coli
4-12 weeks: S. pneumonia, group B strep
3 months - 18 years: s pneumonia, n meningitidis (rash)
18 - 50: s. pneumoniae, n meningitidis
>50: S pneumoniae, n meningitidis
68
Q

gram positive endospore forming rods

A

clostridium botulinum: descending paralysis (neurotoxin blocks release of ACh)
C. perfringens: gas gangrene, multi toxins causing necrosis of tissues.
C. tetani: blocks GABA and glycine so muscle tetani.
C. defficile: pseudomembranous colitis: diarrhea with mucus after antibiotics

69
Q

Gm positive endospore forming rods

A

B cereus: GI and eye infections (food poisoing in baked goods, fried rice)

B anthracic: black eschar formation, inhalation of spores from soil, animals, halo around heart

70
Q

gm + non spore formers

A

corynebacterium diptheriae: diptheria, skin and resp secretions

  • viral URI and c diptheriae jumps on with virus and invades throat.
  • greyish pseudomembrane which is necrotic tissue

Listeria monocytogenes: tiny rod, animals, goes to heart and brain

  • immunocompromised
  • dangerous in pregnancy (granulomatosis infantiseptica)
71
Q

gram negative rods

A 
oxidase negative, faculatative anaerobes, ferment glucose
E. coli
salmonella
shigella
klebsiella
yersinia
enterobacter aerogenes
citrobacter freundii
proteus
pseudomeonas aeurguinosa
legionella pneumophilia
72
Q

gram negative rods

E. coli

A

E. coli: most common, ferment lactose (shigella and salmonella do not)
- septicemia
- UTI
- gastroenteritis
- neonatal meningitis (group B strep is #1)
enterotoxigenic: sm intestine, travelers diarrhea
enteropathogenic: sm intestine infantile non-bloody diarrhea
enteroinvasive: large intestine epithelial invasion, water diarrhea followed by dysentery w scant bloody stools
enterhemorrhagic E. coli (0157:H7): verotoxin (shigella like toxin)
- hemorrhagic colitis, severe N/D, copius diarrhea, with bloody phase, DIC, most common in children under 5. HUS
***toxin producer and 0157:H7 can makes all E. coli in gut to produce toxin.

73
Q

gm negative rods

A

e.coli
salmonella typhii: associated with rose spots on abdomen
salmonella enteritidis: found on egg shells, rapid onset
shigella: pus/bloody diarrhea, lower abd cramps, toxin mediated (shiga toxin), common from food handlers (4 F’s fingers, food, feces, flies)

74
Q 
gm negative rods
klebsiella
enterobacter aerogenes
citrobacter freundii
yersinia
A

klebsiella: current jelly sputum, immunocompromised, lobar pneumonia
enterobacter aerogenes: immunocompromised
citrobacter freundii: immunocompromised
yersinia pestis: plague, bipolar staining,
yersinia enterocolitica: proximity to animals, apendicitis like symtoms

75
Q

gm negative rods
proteus
psedamonas
legionella

A

proteus: urea splitters, urine pH is higher = more stones
pseudamonas aeruginosa: everywhere, burn infections, antibiotic resistant
legionella: flu-like, pontiac fever, cruise ship, standing water and potting soil

76
Q

gm neg curved rod
h pylori
campylobacter jejuni
vibrio cholera

A

h pylori: precursor for adenocarcinoma in stomache, gastric ulcer, urease producer

campylobacter: shell fish vector, immunocompromised, fecal oral, RLQ pain, most common cause of bacterial enteritis in US
vibrio: mild severe diarrhea, rice water stools, fluid loss kills

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