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Foundations Exam 3 > Gram- Rods Causing GI Disease > Flashcards

Gram- Rods Causing GI Disease Flashcards

1
Q

What family of bacteria does this describe: short thick rods, peritrichous flagella (all around the outside), and oxidase negative?
a. Enterobacterales
b. Vibrio
c. Campylobacter

A

a. Enterobacterales (previously Enterobacteriaceae): short thick rods, peritrichous flagella, oxidase negative

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2
Q

what is the shape of Vibrio bacteria? are they oxidase positive or negative?

A

Vibrio: curved rods with polar flagella (flagella sticking out from one side like a tail), oxidase positive

(Gram- rod)

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3
Q

what shape are Campylobacter and Helicobacter bacteria?

A

curved or spiral shape

(Gram- rod)

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4
Q

what are the four 4’s of oral-fecal transmission?

A

Feces
Fingers
Flies
Food (& water)

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5
Q

M cells of intestine

A

specialized for transcytosis of antigens to underlying lymphoid tissue - many pathogens “hitch a ride” to exit intestine

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6
Q

H, O, and K bacterial antigen (used in stereotyping)

A

H = flagella
O = LPS
K = capsular (“kapsule”)

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7
Q

what is the difference in nature of intestinal infection conferred from Vibrio vs Shigella vs Yersinia? (all Gram- rods)

A

Vibrio and some E. coli —> bacteria secrete toxins but remain in intestinal lumen

Shigella and non-typhoidal Salmonella —> bacteria invade intestinal wall

Yersinia and S. typhi —> bacteria invade beyond intestinal wall and cause systemic infection

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8
Q

Which of these bacteria is most likely to cause systemic infection?
a. Vibrio
b. Yersinia
c. non-typhoidal Salmonella
d. Shigella

A

b. Yersinia: invades beyond intestinal wall and causes systemic infection

note these are all Gram- rods which all cause intestinal infections
a. Vibrio - secrete toxins but remain in lumen
c. non-typhoidal Salmonella and (d.) Shigella - bacteria invade intestinal wall

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9
Q

describe the pathology of non-invasive enteritis (name key virulence factors)

A

virulence factors: adhesions and exotoxins —> stimulate salt transport —> osmotic outflow of water follows —> watery diarrhea (with or without wbc)

[remember that exotoxins are deliberately secreted, vs endotoxins which are released upon lysis]

*examples: Vibrio cholerae, toxin-producing E. coli

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10
Q

Vibrio cholerae and toxin-producing E. coli are similar in that they both cause what kind of enteritis? (Gram- rods)

A

non-invasive enteritis:

virulence factors: adhesions and exotoxins —> stimulate salt transport —> osmotic outflow of water follows —> watery diarrhea (with or without wbc)

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11
Q

what is the specialized media that Vibrio cholerae grow on? (Gram- rod)

A

Thiosulfate Citrate Bile Salt (TCBS) agar - appear as bright yellow colonies on background of green (normal flora)

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12
Q

what is the function of the A and B subunits of Cholera toxin?

A

A subunit: adds ADP-ribose to Gs protein to constitutively activates it —> adenyl cyclase —> high cAMP —> high Cl- transport (via CFTR transporter) —> osmotic outflow of water into lumen —> watery diarrhea

B subunit: pentamer, mediates attachment to enterocytes

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13
Q

why is it thought that cystic fibrosis heterozygotes are more resistant to diarrhea from Cholera toxin (of Vibrio cholerae, Gram- rod)?

A

Cholera toxin is made of A and B subunit

A: adds ADP-ribose to Gs (permanently active) —> cAMP —> high Cl- transporter via CFTR —> high salt concentration in lumen pulls water out osmotically —> watery diarrhea

(B subunit mediates attachment to enterocytes)

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14
Q

How is enteritis from Vibrio cholerae (Gram- rod) infection treated?

A

fluid replacement (oral or IV) for massive diarrhea

tetracycline or ampicillin can shorten disease

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15
Q

name 2 non-cholera Vibrio bacteria (Gram- rods) and describe where they are found and what illness they cause

A
  1. V. vulnificus
  2. V. parahaemolytics
  • found in natural waters
  • diarrhea from eating raw fish/shellfish
  • wound/soft tissue infections
  • require NaCl for culture (halophiles)
  • grow on TCBS medium (thiosulfate-citrate-bile salts)
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16
Q

what do Vibrios vulnificus and Vibrios parahaemolytics require for culture? (Gram- rods)

A

both are non-cholera Vibrios common in natural waters - can cause diarrhea (raw fish) and wound/soft tissue infections

halophiles: require NaCl for culture
grow on TCBS medium (thiosulfate-citrate-bile salts)

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17
Q

halophiles

A

bacteria that require NaCl for culture

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18
Q

what are the 3 categories of E. coli, based on differences in virulence factors?

A
  1. Enterotoxigenic E. coli (ETEC): “travelers diarrhea” (most adults immune to their own local ETEC)
  2. Enteropathogenic E. coli (EPEC): Type III secretion system causes cytoskeletal rearrangement, loss of brush border (“attaching and effacing lesion”)
  3. Shiga toxin-producing E. coli (STEC): inflammatory enteritis, hemolytic uremic syndrome (HUS)
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19
Q

what toxins cause disease in enterotoxigenic E. coli (ETEC)? (2)

A

adhere to intestinal mucosa via pili

  1. Labile Toxin (LT): similar to cholera toxin
  2. Stable Toxin (ST): structural analogue of gut peptide hormone, stimulates guanyl cyclase-coupled receptor (increases cGMP)

elevated cAMP or cGMP —> diarrhea (less severe than in cholera due to less toxin produced)

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20
Q

how does the severity of diarrhea from enterotoxigenic E. coli (ETEC) compare to Vibrio cholerae? (Gram- rods)

A

the Labile Toxin (LT) resembles cholera toxin but less is produced, so diarrhea is less severe

patients typically do not require hospitalization and intensive rehydration

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21
Q

describe the pathogenic mechanism of Enteropathogenic E. coli (EPEC)

A

adhere to surface of enterocytes, Type III secretion system exports proteins into cytosol and rearranges cytoskeleton - creates pedestal that cups bacterium produced

attaching and effacing lesion - brush border disappears (tight junctions disrupted) —> leakiness causes diarrhea (not directly toxin-mediated)

22
Q

describe the pathogenesis of infection by bacteria that invade the intestinal wall (such as Shigella, Salmonella, invasive E. coli, Campylobacter)

A

virulence factors: adhesions, cytotoxins —> bacteria invade/kill enterocytes, induce their own phagocytosis via Type III secretion system

diarrhea from local production of inflammatory mediators (enterocytes, neutrophils) - may be bloody with wbc present

exotoxins can have systemic effects

23
Q

what type of bacteria does this describe?
- infects humans only
- very low infectious dose
- almost identical to E. coli, but typically cause more severe disease

A

Shigella (Gram- rod)

24
Q

describe the clinical manifestation of Shigella infection (Gram- rod)

A

Bacillary dysentery: frequent, painful, low-volume stools containing blood, WBC, mucus, cramps

25
Q

name the 4 species of Shigella, as defined by O-antigen (LPS), and indicate which is most and least virulent

A
  1. S. dysenteriae: most virulent, but least common
  2. S. flexneri
  3. S. boydii
  4. S. sonnei: least virulent, most common
26
Q

describe how Shigella (Gram- rod) invades and kills cells of intestinal mucosa

A

transcytosis by M cells —> Type III secretion system to invade enterocytes —> lyse phagocyte vacuole —> induce actin polymerization —> actin tail pushes bacteria into adjacent cells

27
Q

describe the structure and mechanism of Shiga toxin

A

AB5 subunit (single A subunit, 5 B subunits)

A subunit cleaves RNA of large ribosomal subunit (inactivates)

systemic effect —> Hemolytic-Uremic Syndrome (HUS) —> microvascular damage in kidneys and hemolysis

28
Q

what kind of illness do STEC cause? (Gram- rod)

A

STEC = Shiga-toxin producing E. coli, basically enteropathogenic E. coli (EPEC) that produce Shiga-like toxin (SLT)

can cause hemorrhagic colitis (then referred to as Enterohemorrhagic E. coli / EHEC)

Shigella-like disease: inflammatory enteritis, hemolytic uremic syndrome (HUS)

29
Q

on what media is Shiga toxin-producing E. coli (STEC) cultured? (Gram- rod)

A

sorbitol-MAC plate —> STEC is sorbitol negative

30
Q

what is the predominant serotype of Shiga toxin-producing E. coli (STEC)? what is the principal host of this serotype? (Gram- rod)

A

O157:H7 - principle host is cattle

31
Q

human infections from non-typhoidal Salmonella mostly come from what foods? (Gram- rod)

A

meat and eggs

(infections with rare serotypes from pet reptiles)

32
Q

what is the human pathogen of non-typhoidal Salmonella? (Gram- rod)

A

Salmonella enterica, which also has many subspecies (such as salamae, arizonae, indica, bongori, etc)

33
Q

what is the pathology of disease from non-typhoidal Salmonella? (what is the general mechanism and what symptoms does it cause)

A

gastroenteritis/enterocolitis

exit lumen via M cells, invade enterocytes, multiply locally

induce apoptosis in macrophages via Type III secretion system

—> non-bloody diarrhea, fever, nausea, vomiting

34
Q

what bacteria is associated with Guillian Barre syndrome? (inflammatory ascending paralysis)

A

Campylobacter jejuni (Gram- rod) - thought to be due to antigen cross-reaction

35
Q

where does Campylobacter jejuni come from, and what does it look like under a microscope?

A

contaminated food (chicken)

“Gullwing” morphology - curvy like seagull (Gram- rod)

requires selective medium (Campy-BAP) and incubation procedure

36
Q

how does Helicobacter pylori (Gram- rod) escape destruction from stomach acid?

A

lives below mucus layer and produces urease (converts urea to ammonia - basic)

causes chronic infection of gastric mucosa, peptic ulcers, stomach cancer

37
Q

what does the pathogenic strain of Helicobacter pylori have that makes it pathogenic?

A

Type IV secretion system - exports cytotoxin

38
Q

how is infection from Helicobacter pylori (Gram- rod) diagnosed?

A

gastric biopsy with visualization of bacteria

“breath test”: patients ingest radiolabeled urea and exhaled CO2 is analyzed by mass spectrometry

current standard of care: stool antigen assay

39
Q

what is the treatment for infection with Helicobacter pylori? (Gram- rod)

A

antibiotics + bismuth salt (Pepto-bismol) + proton pump inhibitor (reduce gastric acid)

40
Q

Yersinia and typhoidal Salmonella are both Gram- rods which invade the intestinal wall to cause systemic infection

contrast the routes by which they spread

A

Yersinia: travels via local lymph nodes

typhoidal Salmonella: travel via blood

41
Q

what are the 2 enteropathogenic serotypes of Yersinia (Gram- rod)? where do they come from, and what illness do they cause?

A
  1. Yersinia enterocolitica
  2. Yersinia pseudotuberculosis

grow in refrigerated foods (milk), blood products

Type III system translocates proteins that inhibit phagocytosis —> inflammation of lymph nodes (mimics appendicitis)

42
Q

what kind of Salmonella is unique to humans, and how does it cause disease?

A

Typhoidal Salmonella - Salmonella typhi (Gram- rod)

Capsule has Vi (virulence) antigen, penetrates intestine via M cells

multiply inside phagocytic vacuole, spreads throughout body (does not cause macrophage apoptosis)

43
Q

how does Salmonella typhi (Gram- rod) spread? where in the body can it be cultured from? Where does it lay dormant?

A

can establish chronic carrier state in gallbladder, and carrier can shed Salmonella for years

may be cultured from blood and bone marrow

44
Q

what 2 agars are typically used for etiologic diagnosis of GI infections? (most importantly used for Shigella and Salmonella)

bonus if you can add how Shigella and Salmonella would appear on these

A
  1. MacConkey Agar: lactose fermenters (pink) vs non-lactose fermenters (yellow)
    [both Shigella and Salmonella are non-lactose fermenters, while most others are lactose fermenters]
  2. Hektoen Enteric Agar: selective for Gram- rods (bile salts) and differential for commensal vs non-commensal
    [Salmonella appears black, Shigella appears pale green, normal flora is pink]
45
Q

how does a triple sugar iron (TSI) slant work?

A

media is hardened at angle so it is slanted in bottle - small amount of glucose, larger amount of lactose and sucrose

stab colony into media - will turn yellow if bacteria can ferment glucose (stays red if not)

if glucose runs out, but bacteria can use lactose and sucrose (2nd choice of fuel) - media will stay yellow (E. coli, Klebsiella, Enterobacter, Yersinia, Serratia)… then if bacteria produces H2S, tube turns black (Proteus)

but if lactose/sucrose non-fermenter - slant of media stays red (Shigella)… then if bacteria produces H2S, tube turns black (Salmonella)

46
Q

what is the drawback of syndromic panels for GI pathogens?

A

culture-independent, so organism cannot thereafter be stereotyped or fingerprinted, which is important for epidemiology and tracking outbreaks

if positive result, lab should go back and get culture for this purpose

47
Q

what are 2 extra-intestinal infections caused by E. coli (Gram- rod)?

A
  1. UTI: cystitis (bladder infection), urgency/frequency/dysuria is classic, diagnosed via quantitative culture and rapid dipstick test for neutrophil or bacterial enzymes; pyelonephritis (kidney infection, via P-fimbrae of bacteria)
  2. Meningitis: via E. coli K1, causes neonatal infections - via S. fimbrae (adheres to choroid plexus), K1 capsule (polymer of sialic acid), iron-acquisition systems
48
Q

what bacterial component of E. coli (Gram- rod) allows adherence to the upper urinary tract epithelium to cause pyelonephritis (kidney infection)?

A

P-fimbrae

49
Q

describe meningitis caused by E. coli (Gram- rod) - what strain causes it, and what 3 virulence factors are important for infection

A

E. coli K1 —> neonatal meningitis

  1. S. fimbrae: adheres to endothelium and choroid plexus
  2. K1 capsule: polymer of sialic acid (non-immunogenic, resembles host so does not activate complement)
  3. iron-acquisition systems
50
Q

nosocomial infections =

A

nosocomial infections = hospital acquired infections

more frequently antibiotic-resistant

common: Enterobacterales, Acinetobacter spp., Pseudomonas aeruginosa, Stenotrophomonas maltophilia

51
Q

this highly encapsulated bacteria has multiple antibiotic resistance mechanisms, and causes necrotizing pneumonia with bloody “currant jelly” sputum. what is?

A

Klebsiella spp. (type of Enterobacterales)

52
Q

this type of Enterobacterale is often multi-drug resistant and produces colonies with red pigment. what is?

A

Serratia

Foundations Exam 3 (28 decks)

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