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Micro/Immuno FINAL > G- pathogens of mucosal surfaces pt.1 > Flashcards

G- pathogens of mucosal surfaces pt.1 Flashcards

1
Q

what enterobacteriaceae are prolific colonizers of mucosal surfaces?

A
  • escherichia coli
  • salmonella spp.
  • shigella spp.
  • klebsiella spp.
  • proteus spp.
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2
Q

what vibrionoaceae are prolific colonizers of mucosal surfaces?

A

vibrio spp.

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3
Q

what is a mucosal surface?

A

surface that interacts with air that has associated glands for secreting mucus

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4
Q

what are some mucosal surfaces?

A
  • oral cavity
  • resp. tract
  • reproductive/urinary tract
  • gastrointestinal tract
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5
Q

what are the defenses of the mucosal surfaces?

A
  • innate immunity
  • adaptive immunity
  • nonspecific barrier defenses
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6
Q

why study gastrointestinal diseases?

A

estimate 76 million cases of intestinal tract infection in the US each year. approx. 500,000 require prolonged hospitalization and 5000 will die

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7
Q

what are ways that gram negative mucosal pathogens are transmitted?

A

feces to mouth via any of the 7 F’s

  1. feces
  2. food
  3. fluids
  4. fingers
  5. flies
  6. fomites
  7. fornication
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8
Q

what does a small inoculum (50-100 orgs) mean?

A

resistant to most defenses on body and can be directly spread from fecal to oral
ex: shigella dysenteriae, EHEC, EIEC

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9
Q

what does a large inoculum (millions of orgs) mean?

A

most of the pathogens are killed but survivors are enough to cause disease
ex: ETEC, EPEC, vibrio spp.

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10
Q

why aren’t we always infected with gram negative pathogens?

A
  • natural barrier defenses: secretory substances, anatomical and physiological barriers, indigenous microbiota
  • innate immunity
  • adaptive immunity
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11
Q

how do natural anatomical and physiological properties assist with creating a physical barrier?

A
  • acidity: pH 1-2 or 9
  • motility: GI from peristalsis, respiratory from microcillia
  • mucous layer and underlying glycolayx
  • tight junction: protein between epi cells so will have to invade across epi cells or between them
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12
Q

T/F: there is only a single layer that separates outside world from inside body from billions of microbes found on all mucosal surfaces

A

T

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13
Q

T/F: bacteria resistant to gastric acid are those with low infectious doses

A

T

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14
Q

why are most pathogens not in upper/middle small intestine?

A

because of motility… they can’t grab onto cells

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15
Q

pathogens colonize which area of the GI tract the most?

A

ileum and colon

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16
Q

T/F: the natural GI flora out compete pathogens for nutrients/binding sites creating a physical barrier to colonization

A

T

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17
Q

when normal microbiota is suppressed is there an incr. or decr. in susceptibility to pathogens?

A

incr.

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18
Q

what effect does lysozyme (muramidase) have as an antimicrobial?

A

cleaves beta 1,4-glycosidic linkages between NAG and NAM therefore more effective against G+ because more peptidoglycan

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19
Q

what effect does lactoferrin have as an antimicrobial?

A

bacteriostatic effects via sequestering iron (binds Fe and keeps it away from bacteria)

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20
Q

what effect does cathelicidin have as an antimicrobial?

A

distrupts bacterial membranes of G+ and G- (as well as fungi)

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21
Q

what effect do defensins have as antimicrobials?

A
  • create pores in microbes (all microbes can be affected)
  • alpha-defensins produced by neutrophils and paneth cells (in intestines)
  • beta-defensins produced by epithelial cells
  • highly expressed on mucosal surfaces
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22
Q

what effect do immunoglobulins have as antimicrobials?

A

secretory IgA on mucosal surfaces to bind/coat pathogens so its harder for them to attached to mucosal tissue

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23
Q

how do pathogenic bacteria overcome these innate barrier defenses?

A
  • acid resistance: microbes with low infectious dose tend to acid resistant (shigella spp. and enteroinvasive e. coli)
  • fimbriae/pili: adhesins adhere to host
  • bacterial structures:
    • G+/G- cell membrane sensitivities to bactericidal compounds
    • cationic amino acids into cell membrane to reduce effects of cationic antimicrobial peptides
    • siderophores to sequester iron in low iron environments (eg enterobactin produced by e. coli)
    • development of capsule to resist phagocytosis
    • development of mechanisms capable of neutralizing the phagocytic compartment of macrophages (reactive oxygen and nitrogen)
24
Q

why are macrophages an important component of mucosal immunity?

A
  • they recognize microbes via PRRs which leads to activation of the macrophages and the ability to kill many microbes
  • this initiates the inflammatory response
25
Q

what do inflammatory cytokines do?

A
  • activate macrophages

- bring in more inflammatory cells due to non-specific recognition of microbes thru PRRs

26
Q

Which TLR is important in G- bacteria?

A

TLR-4: binds G- bacteria LPS

27
Q

what is the negative side effect to initiating the inflammatory response at mucosal surfaces?

A

inflammatory cytokines such as TNF-alpha can disrupt the tight junctions between epithelial cells

28
Q

where are the densest clusters of lymph nodes found?

A

near mucosal tissues

29
Q

which immune response is generated in the lymph nodes?

A

the adaptive immune response

30
Q

what are the 3 ways that toxins cause disease?

A
  1. invasive bacterial pathogens
  2. toxin-producing bacterial pathogen
  3. “hybrid” misfits
31
Q

describe invasive bacterial pathogens?

A
  • ex: salmonella spp, shigella spp.
  • large intestine
  • small volume of stool
  • bloody stool
  • leukocytes in stool
  • tissue ulcerations
32
Q

describe toxin-producing bacterial pathogens?

A
  • ex: vibrio spp (but primarily v. cholerae), enterotoxigenic e. coli (ETEC)
  • small intestine
  • copious amounts of watery stool
  • no blood in stool
  • no leukocytes in stool
  • no tissue damage
33
Q

describe “hybrid” misfit pathogens?

A
  • ex: enterohemmorhagiv e. coli (EHEC) and enteropathogenic e. coil EPEC)
  • lower small intestine/upper large intestine
  • colonization causes attaching and effacing lesion
  • blood in stool (and possibly in urine with EHEC)
  • change leads to water loss and produces toxin
34
Q

there are four species of shigella distinguished by which antigen?

A
  • O antigen
    1. s. dysenteriae
    2. s. flexneri
    3. s. boydii
    4. s. sonnei (in USA)
35
Q

is the shigella inoculum size very large or small?

A

small

36
Q

what facilitates shigella’s survival through the stomach?

A
  • acid resistance which is controlled by a global regulatory system of genes under the control of RpoS made in the stationary phase. occurs when shigella are grown anaerobically
  • genes triggered help with acid resistance because of anaerobic environment. once reach acid environment start expressing genes for invasion
37
Q

where does shigella multiply/colonize?

A

distal part of terminal ileum and colon because its anaerobic

38
Q

how do Shigella spp. invade?

A
  1. mucosal surface is resistant to infection, but basal surface is not
  2. enter M cells, via outer membrane proteins called invasive plasmid antigens
  3. released into lamina propria, ingested by macrophages. inflammatory response causes illness
  4. epithelial cells will ingest the bacteria, facilitated by bacterial factors
  5. bacterial proteins lyse the phagosomal vesicle so can go from one epi cells to next
  6. intracellular spread facilitated by IcsA, an ATPase that causes actin polymerization

-only a few Shigella need to be passed through

39
Q

what damage is done from Shigella invading?

A
  • an ulcer develops when invaded cells die and slough off
  • neutrophils can be seen by microscopy in stool samples
  • all species will induce an inflammatory diarrhea with leukocytes in the stool.
  • S. sonnei induces a watery stool (still has leukocytes) = EXCEPTION
40
Q

why is Shigella dysenteriae type 1 different?

A
  • gastroenteritis caused by S. dysenteriae type 1 presents as an invasive diarrhea
  • S. dysenteriae type 1 also produces Shiga toxin
41
Q

what does Shiga toxin do?

A
  • kills intestinal epithelial and endothelial cells
  • disrupts Na absorption
  • more pronounced watery/bloody diarrhea
42
Q

name and briefly describe the 4 types of infections caused by salmonella.

A
  1. gastroenteritis: typhimurium and enteritidis serovars; chicken meat, eggs, dairy products
  2. focal infection of vascular endothelium: cholerasuis and typhimurium
  3. infections of organ systems: typhimurium
  4. typhoid fever: typhi and paratyphi; human carrier state, high mortality, bacteremia and multiorgan dysfunction
43
Q

how is salmonella infection transmitted?

A

fecal (human or animal)- oral transmission

44
Q

does salmonella need a large or small inoculum size?

A

large

45
Q

is salmonella more or less acid sensitive than shigellae?

A

MORE

  • low pH induces the expression of at least 40 proteins found on pathogenicity islands on large virulence plasmids
  • acidity in stomach triggers these genes
46
Q

how do salmonella spp. invade?

A
  1. when orgs approach the cell’s surface, they induce activity of cell signaling pathways, and cause an incr. in cellular Ca2+
  2. these events induce surface “ruffles” and uptake of the orgs (microbe-directed phagocytosis)
  3. remain within cell vesicles for many hours (unlike Shigella)
  4. orgs released to lamina propria somehow induces NaCl loss from the host cells
  5. macrophages engulf host, but some escape to cause transient bacteremia
    - typhoid serovars will survive and grow in macrophages
47
Q

where are macrophages located for mucosal immunity?

A

directly under epi cells and will control salmonella replication present to adaptive immune system

48
Q

specifically how does salmonella typhi cause typhoid fever?

A
  • enters into lymphatic system

- replicates within macrophages throughout the body

49
Q

can salmonella typhi replicated in animals?

A

no, strictly a human pathogen

50
Q

how are typhoid mary’s or salmonella asymptomatic carriers ID’ed to carry it?

A

carriers have colonized gall bladders and the organisms can be cultured from their feces

51
Q

salmonella typhi replicates where?

A
  • liver
  • spleen
  • bone marrow

**unique property of the strains that cause typhoid fever

52
Q

what are some similarities between shigella and salmonella?

A
  • both are invasive, so both cause invasive diarrhea not much stool but bloody (neutrophils)
  • both are able to respond to environmental changes (acid or anaerobic environment)
53
Q

what are some dissimilarities between shigella and salmonella?

A
  • inoculum size
  • bacteremia
  • species that cause severe disease are very dissimlar
54
Q

how are invasive enteric pathogens ID’ed?

A

based on symptoms and based on stool cultures

55
Q

what is the treatment recommended for invasive enteric pathogens?

A
  • oral rehydration (always a good idea)
  • most of the time no treatment because gets better within week
  • antibiotic resistance first ID’ed in Shigella: fluoroquinolones, beta-lactams
  • salmonella gastroenteritis: antibiotics not indicated by 2nd generation fluoroquinolones can be used
  • typhoid fever/typhoid mary: fluorquinolones or surgical removal of gallbladder, vaccine to the capsule of s. typhi

Micro/Immuno FINAL (16 decks)

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