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Block 4 Found Sci > VI- GI Bacterial > Flashcards

VI- GI Bacterial Flashcards

1
Q

1-8 hour bacterias

A
  1. Staph aureus
  2. Bacillus cereus (emetic)
  3. Clostridium botulinum

aka have preformed toxins

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2
Q

8-16 hour bacterias

A
  1. bacillus cereus (diarrheal)
  2. clostridium perfringens
  3. clostridium botulinum

toxins are produced in vivo

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3
Q

16+ hour bacterias

A
  1. shigella spp
  2. salmonella spp
  3. listeria monocytogenes
  4. E. Coli
  5. campylobacter spp
  6. vibrio

attachment, growth, and virulence factors produced

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4
Q

general presentation of food poisoning

A
  1. diarrhea
  2. vomitting
  3. NO FEVER
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5
Q

bacterias that give food poisoning

A
  1. Staph. aureus
  2. Clostridium botulinum
  3. clostridium perfringens
  4. Bacillus cereus
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6
Q

Staph. Aureus presentation

A
  1. severe vomiting, diarrhea, abdom pain within 1-8 hours
  2. resolves in 24 hours
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7
Q

Staph. Aureus toxins

A

ingestion of preformed enterotoxins (A most common) that are all heat stable aka will survive cooking

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8
Q

foodborne botulism presentation

A
  1. non specific signs less than 8 hours after toxin or 16 hours of spore ingestion
  2. 1-3 days later affect cranial nerves so bilateral ptosis, ophthalmoplegia, blurred vision, dilateral descending weaking > flaccid paralysis
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9
Q

Clostridium botulinum toxin

A

botulism toxin
-ingestion of either preformed toxin or spores that germinate in intestine
-directly causes flaccid paralysis by binding motor end plates of muscle fibers

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10
Q

foodborne botulism treatment

A

IV anti-toxin ASAP to stop progression of paralysis + ventilation for respiratory dysfunctions + supportive therapy

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11
Q

infant botulism presentation

A

ingestion of spores from honey or contaminated formula between birth - 6 mo

constipation, weak cry, failure to thrive, flaccid paralysis so floppy baby

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12
Q

C. perfringens presentation

A
  1. diarrhea and abdom cramps 8-16 hours after ingestion
  2. last for 24 hours

from enterotoxin

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13
Q

emetic Bacillus cereus features

A
  1. from reheated rice
  2. ingest preformed heat stable toxin
  3. onset 15 min - 8 hrs
  4. vomiting, nausea, abdom cramps, NO DIARRHEA
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14
Q

diarrheal Bacillus cereus features

A
  1. meat, veggies
  2. spores germinate in intestine, heat liable toxin
  3. onset 8-16 hours
  4. diarrhea, nausea, abdom cramps, NO VOMIT
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15
Q

H. pylori characteristics

A
  1. gram neg flagellated curved rod
  2. microaerophilic, like 5% oxy
  3. exclusive to humans
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16
Q

H. pylori presentations

A
  1. gastritis
  2. ulcers
  3. stomach cancer
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17
Q

gastritis prez

A

feeling fullness, upset stomach, nausea, vomiting

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18
Q

ulcers prez

A

dull stomach pain, heart burn, nausea, vomit, stomach bleeding
BLACK OR TARRY STOOLS

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19
Q

H. pylori pathogenesis

A
  1. flagella based motility penetrates gastric mucosa and adhere to epithelium
  2. powerful urease enzyme to convert urea to ammonia = inc toxic levels
  3. VacA for accumulation of vacuoles
  4. CagA oncogenic protein by T4SS
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20
Q

H. pylori diagnosis

A
  1. urea breath test - detect CO2 via gas chromatography if urease present
  2. biopsy
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21
Q

H. pylori treatment

A
  1. antibiotics
  2. proton pump inhibitor or antacid to control acid and prevent further mucosal damage
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22
Q

non inflammatory bacterias

A
  1. EPEC
  2. ETEC
  3. vibrio cholerae
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23
Q

inflammatory ish bacterias

A
  1. listeria monocytogenes
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24
Q

inflammatory bacterias

A
  1. EHEC
  2. salmonella spp
  3. campylobacter
  4. shigella spp
  5. C. difficile
  6. vibrio parahaemolyticus
  7. yersinia enterocolitica
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25
Q

MacConkey positive

A

red colonies
-lactose fermentation
-E. Coli

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26
Q

MacConkey agar negative

A

white or translucent colonies
-salmonella, shigella

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27
Q

indole positive

A

red color change - indole production
-E. Coli, Vibrio spp

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28
Q

indole negative

A

no color change
-salmonella

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29
Q

hydrogen sulfate production black colonies

A

Salmonella (typhi and NT) bc H2S producer
-shigella is not black bc not produce H2S

use Hektoen agar or SS agar

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30
Q

intestinal pathogenic E. Coli’s

A
  1. ETEC - enterotoxigenic
  2. EHEC - enteropathogenic
  3. STEC - shiga toxin producing
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31
Q

ETEC features

A
  1. LT and ST toxins cause electrolyte loss
  2. @ small intestine
  3. travelers, infants
  4. watery diarrhea
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32
Q

EPEC features

A
  1. A/E lesions, loss of microvilli, NO TOXINS
  2. small intestine
  3. infants and peds
  4. watery diarrhea
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33
Q

EHEC features

A
  1. A/E lesions, Stx production (shig toxin)
  2. @ large intestine
  3. bloody diarrhea, HUS sequelae (kidney)
34
Q

EPEC adhesions

A
  1. BfpA - bundle forming pilus
  2. intimin on bacterial surface
  3. T3SS injects Tir into host so can bind intimin to adhere
35
Q

ETEC toxins

A
  1. LT = heat liable toxin, inc cAMP, AB toxin
  2. ST = heat stable toxin, inc cGMP, non AB so does not enter cell

adherence via pili

36
Q

vibrio cholerae diseases

A

gastroenteritis

37
Q

vibrio parahaemolyticus diseases

A
  1. gastroenteritis
  2. bacteremia
  3. wound infection
38
Q

vibrio cholerae presentation

A
  1. asymptomatic to severe watery diarrhea RICE WATER STOOL
  2. 2-3 day incubation, 7 day duration

can kill within hours from dehydration

39
Q

vibrio cholerae epidemiology

A
  1. spread easily thru contaminated water
  2. long term immunity from O antigen
  3. associated with natural disasters, pop displacement, poor sanitary conditions
40
Q

vibrio cholerae toxin

A
  1. Tcp for adherence to enterocytes
  2. cholera toxin = massive fluid efflux, AB toxin that inc cAMP, encoded on prophage
41
Q

vibrio cholerae treatment

A

rehydration therapy IV and oral, no antibiotics
-prevent transmission with clean water and proper sanitation
-oral vaccines but not great

42
Q

listeria monocytogenes survival traits

A
  1. intracellular pathogen
  2. wide growth range
  3. resistant to high salt concentrations
  4. wide pH range
43
Q

listeria monocytogenes presentation

A
  1. healthy - asymp or non specific
  2. immunocomp - bacteremia, meningitis, encephalitis (stiff neck, persistent headache
  3. pregnant women - non specific but risk of transmission to neonate
44
Q

fetal listeriosis

A
  1. early onset - premature babies with flu like illness before delivery mother, in utero infection, onset 0-7 days after birth, blood infection + pneumonia + meningitis
  2. late onset - full term, mo no sign of illness, unclear infection, 5-30 days onset, blood infection + meningitis
45
Q

listeria pathogenesis

A
  1. internalin A protein to mediate adherence and induce uptake
  2. listeriolysin O LLO disrupts vacuole membrane so can escape to cytosol for rep
  3. ActA allows intracellular motility to disseminate liver/spleen/CNS, jet packs
46
Q

listeria diagnosis

A

culture from normally sterile sites (blood, CSF)
1. cold enrichment selectin
2. weak beta hemolysis blood agar
3. pos motility test

47
Q

listeria treatment

A
  1. antibiotics
  2. properly cook animal products, ready to eat meats, wash raw veggies
48
Q

EHEC found in

A
  1. hamburgers, ground beef
  2. raw veggies or fruit
49
Q

EHEC presentation

A
  1. hemorrhagic colitis aka bloody diarrhea
  2. little to no fever
  3. marked abdom tender
  4. HUS sequelae (hemolytic uremic syndrome) so anemia and kidney failure
50
Q

EHEC toxin

A

shiga toxin (AB toxin) that inhibits protein syn > cell death = bloody diarrhea

51
Q

EHEC diagnosis

A

does not ferment sorbitol so will be colorless on MacConkey’s culture

52
Q

EHEC treatment

A

supportive therapy only NOT antibiotics bc may be harmfuul by inc toxin production

53
Q

Salmonella Typhi characteristics

A
  1. gram neg facultative anaerobe
  2. motile flagellated rods with H antigen
  3. intracellular pathogen
  4. highly adapted to humans, humans only reservoir
54
Q

S. Typhi presentation

A
  1. fever with headache, rises over 3 days
  2. fever persists for 4 weeks
  3. infection of gall bladder > reinfection of intestine so diarrhea

rise in rever coincides with rise of pos blood cultures

55
Q

S. Typhi pathogenesis

A

adheres to M cells and enterocytes
-causes apical membrane of M cell to ruffle indicating endocytic uptake
-M cells @ ileum for immune presentation

56
Q

S. Typhi pathogenesis

A
  1. T3SS mediates uptake into M cells + injects Ssps salmonella invasion proteins
  2. Vi antigen polysac capsule promotes extended intracell rep
  3. LPS endotoxin induces fever from septicemia
57
Q

S. Typhi diagnoses

A

culture stool and blood
-white on MacConkeys (non lactose fermenting)
-black on SS or Hektoen agar (prod H2S)

58
Q

S. Typhi treatment

A
  1. antibiotic therapy
  2. avoid sources of infection (drink bottled water in endemic areas, no ice, fully cook veggies, avoid raw fruits/veggies)
  3. vaccination for travelers
59
Q

nontyphoidal salmonella presentation

A
  1. nausea + vomit + abdom cramps
  2. diarrhea - can be loose or severe dysentery with blood/pus for 3-4 days
  3. maybe fever (50%)
60
Q

NT salmonella pathogenesis

A
  1. like S. typhi with T3SS into M cells then ruffles
  2. enter macrophage and kill rapidly by massive inflammatory resp
  3. can disseminate and show focal infections like arthritis, endocarditis
61
Q

NT Salmonella diagnosis

A
  1. white on MacConkeys bc not ferment lactose
  2. black precipitate on hektoen agar bc produces H2S
62
Q

NT Salmonella treatment

A
  1. supportive
  2. NO antibiotics bc can induce carrier state unless severe case
63
Q

Camp. jejuni features

A
  1. sea gull shaped curved rods
  2. motile with flagella
  3. microaerophilic
  4. grow at 42 celcius
64
Q

Camp. jejuni presentation

A
  1. low abdom pain
  2. fever
  3. diarrhea (watery or pus/blood)
  4. complicate to guillain barre syndrome
65
Q

Camp. jejuni pathogenesis

A
  1. flagella mediated adherence to intestinal epithelium
  2. produce toxins
  3. cause acute inflamm, crypt abscess, entry into bloodstream from intestine
66
Q

vibrio parahaemolyticus presentation

A

SHELL FISH
1. common- watery diarrhea, nausea, vomit, abdom cramps, some fever/chills
2. dysentery- severe cramps, nausea, vomit, bloody stools

67
Q

Vibrio. para pathogenesis

A

two major hemolysin toxins
-thermostable direct hemolysin

68
Q

yersinia enterocolitica features

A
  1. bi polar safety pin staining on giemsa
  2. gram neg coccobacilli
69
Q

yersinia entero presentation

A
  1. weeks of abdom pain and cramps
  2. diarrhea - water to bloody
  3. acute mesenteric lymphadenitis - can be confused with acute appendicitis

pork

70
Q

yersinia entero diagnosis

A
  1. NAAT
  2. culture
71
Q

C. diff features

A

spores!
gram pos anaerobe

72
Q

CDAD

c. diff associated diarrhea

A
  1. watery diarrhea with leukocytes and occult blood
  2. nausea, anorexia, fever, dehydration, leukocytosis left shift
  3. abdom distension, tenderness
  4. diffuse or patchy nonspecific colitis
73
Q

pseudo membrane colitis

A
  1. profuse watery diarrhea with leukocytes and occult blood
  2. same CDAD symps but more severe
  3. marked abdom distension, tenderness
  4. adherent yellow plaques
74
Q

fulminant colitis
C-Diff

A
  1. severe OR diminished diarrhea, needs surgery
  2. lethargy, fever, tachycardia, dilated colon
  3. acute abdom sudden/severe/pain
  4. no sigmoidoscopic exam
75
Q

C.diff pathogenesis

A
  1. antibiotics alter/destroy normal intestinal microbiota
  2. c.diff survive then germinate in open niches
  3. toxin A and B produced
  4. mucosal cell injury and inflamm
76
Q

C.diff tests

A
  1. EIA test for toxin A, B or both in stool
  2. glutamate dehydrogenase detection
  3. NAAT/PCR for toxin B
77
Q

c.diff treatment

A
  1. initial infection/1st recurrence use antibiotics
  2. 2nd recurrence or if antibiotic resistance then different antibiotic or fecal microbiota transplant

in isolation NO hand santizer bc not work

78
Q

shigella epidemiology

A
  1. extremely low infectious dose
  2. incidence directly related to hygiene so poor sanitary, crowded healthcare system, day cares
79
Q

shigella presentation

A
  1. majority will be fever + malaise+ watery diarrhea from S. sonnei
  2. can be dysentery with freq feeling need to defecate (tenesmus) from S. flexerni or S. dysenteriae
80
Q

shigella pathogenesis

A
  1. T3SS uptake into M cells
  2. phagocytosed by macrophages
  3. rapid escape from phagosome and induce macrophage apoptosis
  4. spread to neighboring cells from actin
  5. ulcers in infected areas

shiga toxin!!

81
Q

shigella treatment

A
  1. rehydration
  2. antibiotics okay to shorten duration of illness
82
Q

enteroinvasive E. Coli all about

A
  1. gram neg facultative anaerobe
  2. milder form of dysentery shigellosis
  3. same patho as shigella but no toxin

not very common

Block 4 Found Sci (67 decks)

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