Anderson Immunology/Microbiology Flashcards
normal flora: acid tolerant organisms in stomach
normal flora: anaerobic bacteria of small intestine
normal flora: lg intestine
stomach: lactobacilli, streptococci
sm intestine: parasites, fungi
lg intestine: bifidobacter, eubacter, enterobacter, peptostreptococci
anterior urethra normal flora vagina skin nose conjunctiva
ant urethra: lactobacilli, cornybacteria, coag - staph
vagina: lactobacilli (staph, strep)
skin: staph, candida, clostridia, acinetobacteria
nose: anaeorobes
conjunctiva: coag - staph
principles of infectious disease
attachment
replication
spread
shedding/elimination
how does body respond to viral vs bacterial infections
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
fungal infections
delayed hypersensitivity reaction
tumors
t-cell response to tumor growth
activate NKs and macrophages
*compare and contrast endo and exotoxins
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
hypothalamic set-point for body temp
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.
what increases the set-point of temperature?
pyrogens
what are the heat-generating mechanisms?
heat loss mechanisms
- increased metabolism, shivering, vasoconstriction (post hypothalamus)
- vasodilation, increased sympathetic outflow to sweat glands (post hypothalamus)
how does body respond to viral infection?
proliferation of lymphocytes and reduction of PMNs
NK and cytotoxic cells
IgG/IgM neutralize viral particles in blood
interferon
chronic viral infection
can result in reduced # of circulation lymphocytes
bacterial infections
PMNs (neutrophils) increase and lymphocytes decrease
see band cells
fungal infection causes what type of response
type 1 IgE response
response to tumors
t-cell response
NK cells
macrophages
endotoxin vs exotoxin
endotoxin: LPS in outer membrane, not denatured by boiling, pyrogenic
exotoxin: protein extracellular, denatured by boiling, form toxoid, high potency
non-specific immunity
physical barrier: skin, mucus membranes, gastric acid and enzymes
physiological barriers: inflammation, phagocytosis (macrophages, monocytes, PMNs, eosinophils, cell death = pus)
which are granular and which are agranular WBCs?
granular: neutrophils, basophils, eosinophils (phils)
agranular: moncytes and lymphocytes
what causes heat (heat generation)
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
hypothalamic set point
thermosensors in hypothalamus keep track of temp
belief of what temp should be (98.6)
- too low: heat generating
- too high: heat loss
pyrogens
increase set point temp
core temp recognized as lower than the new set-point temp by ant hypothalamus
induce cytokines
what is the trigger for fever?
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
how does aspirin reduce fever?
inhibits cyclooxygenase which inhibits production of prostaglandins and decreases set point
heat exhaustion vs heat stroke
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.
NK cells
non-specific
cytotoxic cells
create hole in ag cell and kill it
stimulated by complement cascade
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
everything matures in ____ except for ____ which mature in the ____
bone marrow
t-cells
thymus
all antibodies come from
B cell response
myeloid stem cells become what?
magakaryocyte -> platelets
proerythroblast -> Reticulocytes -> RBCs
monoblast -> WBCs
myeloblast
what do lymphoid stem cells make
t-cells
cell mediated immunity (kill other tissues or cells)
humoral immunity
cells that produce ab that inactivate invader
NK cells (just kill)
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
monocytes vs macrophages
mono in blood
mac in tissue
- both are phagocytic
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
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
TNF
immune stimulating cytokine
extrinsic pathway for triggering apoptosis.
tumor necrosis factor = TNF alpha
IL - 1
triggers fever
secreted by macrophages and monocytes
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
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
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
first response immunoglobulin
IgM
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
IgA
secretory
tears, saliva, mucus
prevents bacteria, viruses, toxin from attaching
IgE
allergy
type-1 immediate hypersensitivity
parasite infection
IgM
first responder short time period B cells produce IgM elevated in acute infection basis for ABO blood type no false positives
IgG
Long term most common focuses NK to their targets passive immunization (gamma globulin injection) crosses placenta
type-1 hypersensitivity reaction
IgE mediated
anaphylaxis
Type II hypersensitivity
ab mediated response
Goodpastures: antiglomerular and antialveolar ab
Type III hypersensitivity
ab/ag complexes
immune complex mediated
serum sickness (reaction to other blood in system)
Type IV hypersensitivity reaction
non- ab
t-cell mediated
TB skin test reaction
Autoimmunity ab reaction
can happen with any hypersensitivity reaction
autoimmune diseases: DiGeorge’s syndrome
thymic hypoplasia
total absence of cell mediated immunity
agenesis of third and fourth pharyngeal pouches
Scleroderma/Systemic Sclerosis
autoimmune
excessive collagen
fibrosis in microvasculature: skin, GI, kidneys, heart, lungs
mask-like face
Lupus (SLE)
autoimmune injury to skin, kidney, serosal membranes
febrile illnesses
type III hypersensitivity
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
beta hemolysis vs alpha hemolysis
beta: complete, more of a problem
alpha: partial
gram positive cocci staph aureus
staph aureus clusters beta hemolytic coagulase positive empitigo tts scalded skin sydrome osteomyelitis
staph food poisoning
enterotoxin
toxin release form ingested staph
4 hours after ingestion
true food poisoning from toxin not staph itself
staph epidermidis
coagulase neg
surgical wound infections
subacute endocarditis
staph saprophyticus
not common
coag neg
UTIs (community aquired)
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)
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
Group D strep
enterococci: URIs and needle sticks
S pneumoniae: pneumonia, sinusitis, otitis media, meningitis
s. viridans: dental work, endocarditis, bacteremia
How does n. gonorrhea avoid specific immune system?
cilia to attach to mucus membranes
anti-human IgA so IgA can’t attack it
N meningitidis
and sx
catalase and oxidase positive
100% fatal if not treated
fever, ha, nuchal rigidity, purpura
infants: no nuchal rigidity, GI symptoms
Waterhouse friedrichsen syndrome
N. meningitidis -> menigococcemia -> waterhouse friedrichson -> high fever, DIC, adrenal destruction
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
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
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
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)
gram negative rods
oxidase negative, faculatative anaerobes, ferment glucose E. coli salmonella shigella klebsiella yersinia enterobacter aerogenes citrobacter freundii proteus pseudomeonas aeurguinosa legionella pneumophilia
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.
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)
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
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
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
