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Anderson Immunology/Microbiology Flashcards

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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
NK cells
non-specific cytotoxic cells create hole in ag cell and kill it stimulated by complement cascade
26
specific immunity
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
27
everything matures in ____ except for ____ which mature in the ____
bone marrow t-cells thymus
28
all antibodies come from
B cell response
29
myeloid stem cells become what?
magakaryocyte -> platelets proerythroblast -> Reticulocytes -> RBCs monoblast -> WBCs myeloblast
30
what do lymphoid stem cells make
t-cells | cell mediated immunity (kill other tissues or cells)
31
humoral immunity
cells that produce ab that inactivate invader NK cells (just kill)
32
full response to ag
APCs present ag to t-cells t-cells stimulate b-cells while attacking ag B cells produce ab ab attacks ag
33
monocytes vs macrophages
mono in blood mac in tissue - both are phagocytic
34
complement
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
Interferon
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
TNF
immune stimulating cytokine extrinsic pathway for triggering apoptosis. tumor necrosis factor = TNF alpha
37
IL - 1
triggers fever | secreted by macrophages and monocytes
38
MHC 1 and MHC 2 | major histocompatability complexes
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
CD 8 T cells
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
CD 4 T-cells
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
first response immunoglobulin
IgM
42
primary and secondary response in humoral immunity
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
IgA
secretory tears, saliva, mucus prevents bacteria, viruses, toxin from attaching
44
IgE
allergy type-1 immediate hypersensitivity parasite infection
45
IgM
``` first responder short time period B cells produce IgM elevated in acute infection basis for ABO blood type no false positives ```
46
IgG
``` Long term most common focuses NK to their targets passive immunization (gamma globulin injection) crosses placenta ```
47
type-1 hypersensitivity reaction
IgE mediated | anaphylaxis
48
Type II hypersensitivity
ab mediated response | Goodpastures: antiglomerular and antialveolar ab
49
Type III hypersensitivity
ab/ag complexes immune complex mediated serum sickness (reaction to other blood in system)
50
Type IV hypersensitivity reaction
non- ab t-cell mediated TB skin test reaction
51
Autoimmunity ab reaction
can happen with any hypersensitivity reaction
52
autoimmune diseases: DiGeorge's syndrome
thymic hypoplasia total absence of cell mediated immunity agenesis of third and fourth pharyngeal pouches
53
Scleroderma/Systemic Sclerosis
autoimmune excessive collagen fibrosis in microvasculature: skin, GI, kidneys, heart, lungs mask-like face
54
Lupus (SLE)
autoimmune injury to skin, kidney, serosal membranes febrile illnesses type III hypersensitivity
55
HIV
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
beta hemolysis vs alpha hemolysis
beta: complete, more of a problem alpha: partial
57
gram positive cocci staph aureus
``` staph aureus clusters beta hemolytic coagulase positive empitigo tts scalded skin sydrome osteomyelitis ```
58
staph food poisoning
enterotoxin toxin release form ingested staph 4 hours after ingestion true food poisoning from toxin not staph itself
59
staph epidermidis
coagulase neg surgical wound infections subacute endocarditis
60
staph saprophyticus
not common coag neg UTIs (community aquired)
61
everyone at dinner party at food that caused it staph aureus food poisoning. Which food caused it?
not cooked or kept cold (bug stays alive at room temp)
62
Group A beta hemolytic strep | Group B beta hemolytic strep
catalase negative chains A: strep through, pharyngitis, scarlett fever, rheumatic fever B: vaginal infections, neonatal
63
Group D strep
enterococci: URIs and needle sticks S pneumoniae: pneumonia, sinusitis, otitis media, meningitis s. viridans: dental work, endocarditis, bacteremia
64
How does n. gonorrhea avoid specific immune system?
cilia to attach to mucus membranes | anti-human IgA so IgA can't attack it
65
N meningitidis | and sx
catalase and oxidase positive 100% fatal if not treated fever, ha, nuchal rigidity, purpura infants: no nuchal rigidity, GI symptoms
66
Waterhouse friedrichsen syndrome
N. meningitidis -> menigococcemia -> waterhouse friedrichson -> high fever, DIC, adrenal destruction
67
``` most likely organism for meningitis: 0-4 weeks: 4-12 weeks 3 months - 18 years 18 - 50 >50 ```
``` 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
gram positive endospore forming rods
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
Gm positive endospore forming rods
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
gm + non spore formers
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
gram negative rods
``` oxidase negative, faculatative anaerobes, ferment glucose E. coli salmonella shigella klebsiella yersinia enterobacter aerogenes citrobacter freundii proteus pseudomeonas aeurguinosa legionella pneumophilia ```
72
gram negative rods | E. coli
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
gm negative rods
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
``` gm negative rods klebsiella enterobacter aerogenes citrobacter freundii yersinia ```
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
gm negative rods proteus psedamonas legionella
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
gm neg curved rod h pylori campylobacter jejuni vibrio cholera
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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